Detail The Components Of A Synapse And Describe The...

Detail the Components of a Synapse and Describe the...
Synapses are an essential and fascinating part of communication within the central nervous system.
They are the transmitters of chemical and electrical messages that cause us to see, feel, move and
much more. The brain consists of around 100 billion neurons, each of which has around 7,000
synaptic connections to other neurons. It has been estimated that a three year old child has 1,000
trillion synapses, and since number of synapses decreases with age until it stabilises in adulthood it
is estimated the average adult has between 100 and 500 trillion synapses.(Wikipedia contributors
(2006). When looking at the brain in this context, you can appreciate the sheer complexity of it and
that looking at the functioning of a single synapse is ... Show more content on Helpwriting.net ...
Figure 2 shows most of these parts as described above. (Rosenzweig, M, R. Breedlove, S, M. &
Watson, N, V. 2005) Figure 2:
http://www.iworx.com/company2/WebToolsCD/Illustrations/synapse/synapse_web2.jpg
Electrical synapses work faster than chemical synapses with almost no time delay involved. This is
because in electrical synapses, the synaptic cleft is only between 2 and 4 nanometres as compared to
the 20 to 40 nanometre cleft in a chemical synapse. Also the presynaptic and postsynaptic
membranes of the electrical synapses have larger channels fixed in them allowing ions to travel
directly from one cell to the other without having to pass through the synaptic cleft, and the
electrical current can travel between presynaptic and postsynaptic membranes with practically no
time delay. This is opposed to the delay of around a millisecond caused by passage through the
synaptic cleft in a chemical synapse, which although is very quick, for neurons is relatively slow.
(Rosenzweig, M, R. Breedlove, S, M. & Watson, N, V. 2005)
In order for information to be transmitted from the presynaptic neuron to the postsynaptic cell, a
series of events needs to take place. This begins when a nerve impulse i.e the result of an action
potential reaches the presynaptic axon terminal or synaptic knob. This results in the synaptic knob
becoming depolarized, that is, more negatively charged thus activating the voltage–gated calcium
channels into opening. Positively
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Glia Function
Glia was know just to be support cells, but scientist have discovered that they serve a bigger purpose
in the function of the nervous system. Three major categories of glia are: astroglia, oligodendroglia,
and microglia.
Neurons contains a fluid known as extracellular fluid which also contains charged particles called
ions. (can be + or –) Ions are located in cytoplasm, which gives neurons an electrical charge when a
neuron is not sending a message, known as the resting potential (–).
Ion channels only allow certain ions in and out of the cell and can open or close depending on input
received from other neurons. When positively charged information (excitatory) is received from
other neurons it is called the action potential, during this phase sodium is allowed through the ion ...
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How is the Nervous System Organized?
Nervous system has two main parts: the central nervous system, which contains the brain and spinal
cord, and the peripheral nervous system, which contains the nerves throughout our body that send
input back and forth between the periphery and the central nervous system.
The peripheral nervous system is made up of two other systems known as the somatic and the
autonomic systems. The somatic nervous system controls all the nerves in our body that respond to
sensory information (touch and pain) and transmits all the information to the brain and spinal cord,
with the help of the central nervous system. The autonomic nervous system is also made up of two
parts: the sympathetic and parasympathetic nervous systems. The only thing they have in common is
that both these systems have nerve cells and axons distributed throughout the body. The sympathetic
system is active during stress, it is also responsible for the "fight or flight" reaction that allows us to
respond to life threatening scenarios. The parasympathetic system is active during the restful times
and it is responsible for controlling our everyday functions when we are not necessarily at

Grip Lab
Glutamate–receptor–interacting protein (GRIP) is the interacting protein which is associated with
AMPAR protein receptor in the postsynaptic cell. Amount of GRIP is associated with AMPAR
receptors can lead to the prediction of activity in the presynaptic cell. AMPAR receptor change
shape to be ready to receive neurotransmitter when GRIP bind. The presynaptic cell contains vesicle
which neurotransmitters are accommodated. When calcium enters the presynaptic cell by calcium
channel, vesicles dock to the presynaptic cell to become ready to release neurotransmitters to the
synaptic gap. Neurotransmitters are released in a packet called quanta. AMPAR receptor has to
change its shape by GRIP to receive the release of quanta in the synaptic ... Show more content on
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The reason of conducting this experiment is to measure how visual activity correlates to how GRIP
protein can alter AMPAR receptor activity in postsynaptic cell that can lead to prediction of activity
of GRIP protein and AMPAR receptor in presynaptic cell. If GRIP is taken out from postsynaptic
cell, plasticity of postsynaptic cell will not alter since ability of the cell to maintain level of activity
even visual input decrease. In postsynaptic cell, GRIP is necessary or responsible for maintaining
activity level of the cell. My position and job in this experiment is to understand and recognize the
GRIP's role and how GRIP regulates the AMPAR receptor in the presynaptic terminal.
This experiment's results and mechanisms relates current medical disease which well known as
autism spectrum disorder (ASD). Symptoms of ASD are difficulty of communication and interaction
with others and inadequate eye contact. When GRIP proteins do not interact with AMPAR receptor,
ASD were developed due to genetic mutation of the GRIP. GRIPs are located on the presynaptic and
postsynaptic cell, but when diagnosing ASD disease, only postsynaptic cell were observed to detect
ASD. The reason I am desiring to predict activity in presynaptic cell is to understand neuron
activity. Knowing that allows to regulate protein and receptor and manipulate the neurons the way
genetics want to cure ASD. If geneticist know how neurons

Happiness : Depression And Happiness
Depression and Happiness in human beings has been studied from multiple fields: psychology,
biology, chemistry, philosophy, and other fields of note. Depression, which is characterized as a
mental disorder, has been attempted to be explained with theories. These theories look at the a
person's environment, genetics, and even the chemical balances of their brain. Neurotransmitters,
chemicals used by neurons to transmit signals, may have a significant impact on a person's mood.
One of these neurotransmitters, Serotonin, has been linked with depression.
A neurotransmitter, or NT, is "a substance produced in and released from a neuron to affect some
aspect of neuronal function without being transported in the blood" (Webster 2002). Neurons are
cells that make up the brain. They communicate with each other through electrical signals to
produce a variety of functions like muscle movement, thoughts, and senses. Each neuron
communicates with other neurons through contact points between the nerve fiber and neuron cell
body. This contact point is called the synapse. It is in this area that neurotransmitters are released
and transferred between neurons. This transfer of neurotransmitters resulting in communication is
referred to neurotransmission. The electrical signals produced by the neurons are the result of
hyperpolarization and depolarization of the neuron's membrane (Giraldi 2017).
The neuron's membrane has a resting potential with concentrations of Na+ and Cl– concentrated on
the outside of the membrane and K+ on the inside of the membrane. With the arrival of an excitatory
impulse, Na+ channels are opened. Na+ ions move across the membrane through these channels
resulting in depolarization. The depolarization creates a chain reaction of propagated action potential
that travels along the membrane of the neuron. This action potential travels to the end of the neuron
where neurotransmitters are released and absorbed by the next neuron in the synapse. This continues
until the message reaches its destination in the brain or nerve ending in the body. This depolarization
is also known as Excitatory Postsynaptic Potential, or EPSP. The depolarization and action potential
is taken away from its threshold by an inhibitory

Chemical Synapse
The chemical synapse allows for the communication between 2 nerve cells when an AP reaches the
end of the axon and the signal subsequently modulates a postsynaptic membrane potential. This
occurs at neuronal connection points – the synapses. These consist of the axon terminals belonging
to the "sender" cell (presynaptic neuron) and the dendritic spine heads of the "receiver" cell
(postsynaptic neuron). Between them lies the synaptic cleft. At the chemical synapse, the electrical
signal (AP) is converted into a chemical signal, in order to cross this synaptic divide. The
extracellular fluid therein poses a physical obstacle for the AP – that is, unless it manages to
temporarily morph into a chemical courier (neurotransmitter). Thereafter, postsynaptic ion channels
(re)turn the latter (in)to its electrical form. To switch the chemical signal off, the neurotransmitter is
removed ... Show more content on Helpwriting.net ...
This triggers a fusion of small vesicles (neurotransmitter containers) with the presynaptic
membrane. The vesicles burst and release the neurotransmitter into the synaptic cleft (exocytosis),
where it travels towards and docks at its specific receptor on the postsynaptic membrane. These
receptors are directly connected to an ion channel, which thereupon opens (lock & key principle). A
Na/K channel, for example, initiates a high influx of Na+ and a slight efflux of K+ ions at the
postsynaptic membrane. The latter then depolarizes and generates an AP – an electrical signal
passed on along a postsynaptic dendrite. But some neurotransmitter like GABA, for example, will
not trigger a postsynaptic depolarization (Dnalc.org, n.d.). When GABA docks at its receptors, K/Cl
channels open. K+ ions flow out of, while Cl– ions enter the cell. Thus, the negative charge inside
the cell increases and the membrane is hyperpolarized. An inhibitory postsynaptic potential is
triggered and an AP

Neuropeptides
Neuropeptides are synthesized in the soma, the cell body of the neuron. These neuropeptides are
along with specific enzymes packed into vesicles in the Golgi apparatus. In these vesicles the
neuropeptides are transported along microtubules in the axon towards the nerve terminal. During the
course of this transportation the neuropeptides, who at this stage is only precursors of the actual
neuropeptides, are modified by the enzymes into their actual neuropeptide form. The vesicles in
which the neuropeptides are stored in once they arrive to the nerve terminal are called large dense–
core vesicles.
These vesicles will release the neuropeptides as a response to large stimuli, meaning stimuli which
give rise to many action potentials. The site of release is closer to the axon than the synapse and the
neuropeptides then have to diffuse toward the synaptic cleft and the ... Show more content on
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The classical transmitters are instead synthesized in the axon terminal while it is only the enzymes
necessary for their synthesis that are produced in the soma and transported along the axon. These
enzymes then act on precursor peptides, which are recycled versions of the neurotransmitter, to
produce the neurotransmitter. The neurotransmitter is then packed and stored in small clear–core
vesicles. Upon release the classical neurotransmitter bind to both GPCRs and ligand–dependent ion
channels. Therefore only the classical transmitters, and not the neuropeptides, can give rise to
excitatory postsynaptic potential (EPSP) and inhibitory postsynaptic potential (IPSP). As the
neurotransmitter is already in the nerve terminal and is later released directly into the synaptic cleft,
the signalling is faster than that of the neuropeptides. Classical neurotransmitters can also be
released as a response to smaller stimuli, with only a few action potentials, while neuropeptides
require stronger stimuli for

Synapses Essay
1. The purpose of the synapse is that it is where chemical signals pass between neurons. The synapse
is the site where a presynaptic terminal ends close to where a receiving dendrite is. It is not a
physical connection between two neurons, which is what most people think. New synapses are
formed in response to life experiences. The longer people live and the more life experiences they
have the more synapses (connections) they have. If you touched a hot stove, as a child and burnt
your hand, you now have a synapse that keeps you from doing that.
2. Neurons help the brain fulfill its functions by conveying information to other neurons. Neurons
use electrical signals to let other neurons know certain information. The electrical signal is then
turned into a chemical signal so that information is able to be passed to another neuron. The neuron
that ... Show more content on Helpwriting.net ...
The blood brain barrier is the layer around the brain which is made up of endothelial cells and
protects the neurons and glial cells in the brain from substances that could potentially harm them.
The function of the blood brain barrier is just that, a barrier that keeps toxins away from the brain.
Unlike some blood vessels in the body, the blood brain barrier keeps away many substances. Only
drugs that are fat soluble can penetrate the blood brain barrier. These include drugs of abuse and
drugs that treat mental and neurological illness. The blood brain barrier is important for maintaining
the environment of the brain for the neurons.
6. An action potential is an electrical impulse that moves along a neuron axon. They enable signals
to travel fast along the neuron fiber. They last less than two milliseconds. When information is
passed between two neurons, the first neuron gets stimulated and then an action potential happens
and the information is in the other neuron. Action potentials result from the flow of ions across the
neuronal cell membrane. Without action potentials information would not get to other

Medullary Reticular Formation Essay
During REM sleep there are numerous output fibers from REM sleep triggering regions that go
towards the medial medullary reticular formation, some of which have synaptic contacts with the
neurotransmitter serotonin, that contain medullary neurons. The efferent pathway that connects to
the pontine REM regions, which have cells of the medial medullary reticular formation, may be
important for moderating sleep–specific inhibitory or excitatory postsynaptic effects in motor
neurons, and silencing medullary serotonin containing cells. In the dorsomedial pontine, some axon
terminals emanate from there that make synaptic contacts with medullary reticular formation cells
that dispatch axons to the hypoglossal motor nucleus. These cells mediate REM sleep–related
inhibitory or excitatory synaptic potentials that occur in motor neurons associated with REM. ...
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The VLPO , also known as the "sleep switch" , as well as the anterior thalamus and basal forebrain
are activated, which inhibits the arousal system. Particularly, the VLPO, GABA and galanin
containing neurons, inhibit and project wake–promoting regions of the ascending reticular system
and descending brainstem arousal neurons. During the activation of cholinergic neurons in the
pedunculopontine and laterodorsal tegmental nuclei, REM occurs. The withdrawal of the aminergic
arousal system produces inhibition during cholinergic activation. As a result, this causes AcH
release, that triggers neural activity increase that features in

Clostridium Tetani Case Study
Identify the disease caused by Clostridium tetani. Describe the generalised structure of a bacterium.
You may include diagrams but must refer to them in the text. Discuss 5 modes of transmission of
microorganism and identify which of these is the most likely mode for Clostridium tetani
The disease caused by clostridium tetani is called tetanus. It's an acute disease caused by the
anaerobic bacterium bacillus (Marieb & Hoehn, 2016). Tetanus is not a contagious disease and the
only means of getting it is from contaminated wounds. Tetanus is an exotoxin disease. An exotoxin
is a substance released by bacteria. Tetanus infection can be transported around the body by the
lymphatic system. This will affect the vascular system first before spreading ... Show more content
on Helpwriting.net ...
Neurotransmitters are chemicals that carry signals between a neuron and the cells of the body. There
are two types of transmission, presynaptic and postsynaptic. presynaptic transmit impulses towards
the synapse and postsynaptic neuron conducts the signal away from the synapse (Marieb & Hoehn,
2016). When a transmission occurs between a presynaptic and a postsynaptic, molecules that are
stored in the synaptic vesicles, are released from the synaptic knob of the presynaptic and into the
synaptic cleft (McKinley, O'Loughlin

Neurophysiology Study: The Peripheral Nervous System
Emily Crocker
Prof. Bauer
Human Physiology
9 September 2015
Neurophysiology Study The Nervous System is a complex system comprised of two parts: The
Central Nervous System and the Peripheral Nervous System. Each system is then comprised of
nerves and specialized cells, called neurons. The function of a neuron is to transmit messages
throughout the body. The brain has approximately 100 billion neurons, ranging in many different
sizes and shapes. Neurons are classified as cells because they have a cell membrane, nucleus,
cytoplasm, and mitochondria, as well as carry out many of the same processes as a cell (i.e protein
synthesis). But, a neuron is unlike a cell in that they have special structures such as dendrites and
axons, communicate through electrochemical processes, and contain special chemicals called
neurotransmitters (instead of hormones). On average, a neuron fires 200 times per second. When it
is not firing, the neuron is at rest. At rest, the neuron has an overall negative charged ... Show more
content on Helpwriting.net ...
If you were to graph the data, you would see spikes at stimulation patterns 8, 15, 16, 21 and 22. This
shows that the action potential was reaching the threshold point at those patterns. It also looked as
though the connection between the different neurons had a domino effect. If neuron A made neuron
X fire, then neuron B would make neuron X fire in the next stimulation pattern and so on (which
might just be a coincidence). But why did the weak exhibitory, and inhibitory neurons show greater
stimulation, and the strong exhibitory and inhibitory neurons make neuron X fire more times?
Overall, neurons A and D had the overall greatest number of fires and neuron D showed the greatest
amount of stimulation. A and D were both excitatory neurons which could explain why the neuron
fired the most times in those

Neural Tissue
Chapter 12: Neural Tissue – An Introduction to the Nervous System
Learning Outcomes
12–1 Describe the anatomical and functional divisions of the nervous system.
12–2 Sketch and label the structure of a typical neuron, describe the functions of each component,
and classify neurons on the basis of their structure and function.
12–3 Describe the locations and functions of the various types of neuroglia.
12–4 Explain how the resting potential is created and maintained.
12–5 Describe the events involved in the generation and propagation of an action potential.
12–6 Discuss the factors that affect the speed with which action potentials are propagated.
12–7 Describe the structure of a synapse, and explain the mechanism involved in ... Show more
rent neurons of PNS
Interneurons – association neurons
Functions of Sensory Neurons
Monitor internal environment (visceral sensory neurons)
Monitor effects of external environment (somatic sensory neurons)
Structures of Sensory Neurons
Unipolar
Cell bodies grouped in sensory ganglia
Processes (afferent fibers) extend from sensory receptors to CNS
Three Types of Sensory Receptors
Interoceptors
Monitor internal systems (digestive, respiratory, cardiovascular, urinary, reproductive)
Internal senses (taste, deep pressure, pain)
Exteroceptors
External senses (touch, temperature, pressure)
Distance senses (sight, smell, hearing)
Proprioceptors
Monitor position and movement (skeletal muscles and joints)
Motor Neurons
Carry instructions from CNS to peripheral effectors
Via efferent fibers (axons)

Two major efferent systems
Somatic nervous system (SNS)
Includes all somatic motor neurons that innervate skeletal muscles
Autonomic (visceral) nervous system (ANS)
Visceral motor neurons innervate all other peripheral effectors
Smooth muscle, cardiac muscle, glands, adipose tissue
Preganglionic fibers
Postganglionic fibers
Interneurons
Most are located in brain, spinal cord, and autonomic ganglia
Between sensory and motor neurons
Are responsible for:
Distribution of sensory information
Coordination of motor activity
Are involved in higher functions
Memory, planning, learning
12–3 Neuroglia
Neuroglia
Half the volume of the nervous

Protocols For Training For The Different Learning Paradigms
and gill withdrawal will be recorded with a transducer connected to efferent vein of the gill with a
silk suture. Protocols for training for the different learning paradigms are shown in Fig 1. We
anticipate that we will observe aging–dependent decrease in the ability to learn as reported in
vertebrates. In order to understand synaptic aging, the above behavioral experiments will be coupled
with electrophysiological measurements of L7MN–LESN connections. Briefly, in the above
preparation, abdominal ganglion is partially desheathed to gain access to measure
electrophysiological properties using sharp electrodes. Similar experiments were performed on R15
neuron in the abdominal ganglia (See Fig 2&3). Specifically, we will measure the resting membrane
potential, resistance and postsynaptic potentials (PSPs) before and after different behavior training
paradigms described above [6,34]. PSPs are a measure of strength of synaptic connections. These
experiments will answer whether during aging (1) passive properties such as basic membrane
resting potential and resistance change and (2) active properties such as excitatory and inhibitory
postsynaptic potentials change.
How does aging affect synaptic plasticity? (Aim1) We will carry out synaptic plasticity
measurements using a reduced preparation containing abdominal ganglia from mature and old
animals. Specifically, we will expose the abdominal ganglion to plasticity–inducing regimens of 5–
HT stimulation examine intermediate–term

8 Factors That Can Influence The Potential On Postsynaptic...
1. The following are 8 factors that can influence the potential on the postsynaptic membrane:
(a) Excitatory Postsynaptic Potentials (EPSPs): EPSPs increase the postsynaptic neuron's likelihood
to generate an action potential by generating a local depolarization. EPSPs result from excitatory
stimuli, such as an excitatory neurotransmitter (Glutamate) released by the presynaptic neuron.
Excitatory stimuli will bind and open ligand–gated Na+ channels, allowing Na+ ions to move inside
a cell down their concentration gradient. The influx of Na+ ions will cause a local depolarization at
the postsynaptic membrane, which if summated can reach threshold and fire an action potential.
(b) Inhibitory Postsynaptic Potentials (IPSPs): EPSPs decrease the postsynaptic neuron's likelihood
to generate an action potential by generating a local hyperpolarization. EPSPs result from inhibitory
stimuli such as an inhibitory neurotransmitter (GABA) released by the presynaptic neuron.
Inhibitory stimuli can bind and open ligand–gated K+ channels and Cl– channels, allowing K+ ions
to move out of a cell and allowing Cl– ions to move into a cell down their concentration gradient.
The influx of Cl– ions and the outflux of K+ ions causes a local hyperpolarization at the
postsynaptic membrane, which reduces the postsynaptic neuron's probability to firing an action
potential.
(c) Temporal Summation: The presynaptic neuron can influence the postsynaptic neuron by
changing the frequency of the stimulus.

Essay about Beh 225 Brain Response of Behavior
Axia College Material
Appendix C
Brain Response of Behavior
Part I
Note: Parts II and III follow below, complete all three.
Run Multimedias 2.3 and 2.4
* Go to the Web site www.prenhall.com/morris. * Click text: Psychology: An Introduction (12th ed.)
* Click "2" on the select a chapter tool bar. * Click Live!Psych on the left hand menu. * Select 2.3
and 2.4.
Write a 350– to 700–word response to the following: Explain the communication process of neurons
in the brain. List some common neurotransmitters and describe their effect on behavior.
<Insert Response Here>
The communication process of neurons in the brain occurs through an electrochemical process.
Neurons pass neurotransmitters ... Show more content on Helpwriting.net ...
Write a 350– to 700–word response identifying the major regions of the brain and what functions of
behavior the systems of each region control.
<Insert Response Here> The brain is a crucial part of the human body. Our abilities to learn,
remember things, and feel emotions are controlled by this very vital organ. Also, the spinal cord is a
crucial part of the central nervous system. The nerves that send messages to the body are located all
throughout the spinal cord. Additionally, within the brain there are three major regions. They are
called the central core, the limbic system, and the cerebral cortex, which has four hemispheres. The
four hemispheres are the occipital lobe, the temporal lobe, the parietal lobe, and the frontal lobe.
Found within the central core region of the brain are five different regions. Each region controls
different behavioral functions within the human body. These regions are called the medulla, pons,
cerebellum, thalamus, and hypothalamus.
The medulla is responsible for many vital functions, such as; the heart rate, the regulation of

respiration, and even the blood pressure flow throughout the body. The pons region of the brain is
responsible for the sleep–wake cycles. This regulates when the body needs to sleep and awakes the
body when it has had enough sleep. The region called the cerebellum controls bodily movement and
also the regulation of the balance in the body and its necessary reflexes. The

Clostridium Tetani: Pathogenic Bacteria
Clostridium tetani is a species of pathogenic bacteria which causes the disease tetanus in humans
(World Health Organisation [WHO], 2008). Bacteria are prokaryotic microorganisms which contain
various structural components. These components include a cell wall and outer membrane which is
discovered by the gram stain procedure (Kratz, 2011). C. tetani are gram–positive bacteria therefore
its cells have a thick wall however they do not possess an outer membrane ("Vaccines and
immunisations," 2015). Other components include flagella which provide cell movement, pili which
permit cell adhesion to surfaces such as host cells, and bacterial capsules also known as glycocalyx
which prevents the cell from phagocytosis (Todar, 2012).
The DNA of bacteria ... Show more content on Helpwriting.net ...
(2011). Epidemiology and prevention of vaccine–preventable diseases. Atlanta, GA: Dept. of Health
and Human Services, Centers for Disease Control and Prevention.
Baxter, D. (2007). Active and passive immunity, vaccine types, excipients and licensing.
Occupational Medicine, 57(8), 552–556. Retrieved from https://www.dnalc.org
Hassel, B. (2013). Tetanus: Pathophysiology, Treatment, and the Possibility of Using Botulinum
Toxin against Tetanus–Induced Rigidity and Spasms. Toxins, 5(1), 73–83. Retrieved from
http://www.mdpi.com/journal/toxins/
Kratz, R. F. (2011). Barron's E–Z microbiology. Hauppauge, NY: Barron's Educational Series.
Marieb, E. N. (2016). Essentials of human anatomy and physiology, (11th ed.). Essex, England:
Pearson.
Marieb, E. N., & Hoehn, K. (2016). Human anatomy and physiology, (10th ed.). Essex, England:
Pearson.
Todar, K. (2012). Structure and Function of Bacterial Cells. Retrieved from
http://textbookofbacteriology.net/structure.html
Vaccines and immunisations. (2015). Retrieved April 11, 2016, from http://www.cdc.gov
World Health Organisation. (2008). Tetanus. Retrieved from http://www.who.int/immunization/

World Health Organisation. (n.d.). Mother–to–child transmission of HIV. Retrieved April 13, 2016,
from

Cognitive Neuron
Cognitive neuroscience is the study of human mind and brain. Therefore, its role is based on the
inference of raw observations that is brain scans. This is because brain scans have the appearance of
physical objects that can be seen and touched. It tempts us to think that we are seeing the raw reality
in brain scans. However, it is a seductive fallacy. The inferential measurement of the brain activity is
actually electroencephalography (EEG) as in positron emission tomography (PET) and other
scanning tools. Therefore, the EEG makes a raw observation of the brain activity of cognition.
Neurons make ten thousand connections and even the input branches of a single neuron may
compute information. Measuring the electrical activity of single neurons is only a tiny sample of a
very complex ... Show more content on Helpwriting.net ...
There a diverse of neurons and out of that many integrate and fire neuron is focused. This neuron is
known to be a classical neuron that accepts input from other nerve cells through its dendrites. The
dendrites branches are with graded membrane potentials. The voltages across the membrane of the
dendrites can have its continuous values. The graded dendritic potentials add up and if the total
voltage over a brief time interval exceeds about –50mV, they trigger a fast travelling spike or action
potential in the axon of the nerve cell (neuron).
The neuron is to send its signal by firing spikes that is by sending action potentials from the cell
body down the axon to the terminal buttons. At the terminals, a neurochemical is released to diffuse
across the small synaptic gap. Then it triggers a postsynaptic potential in the neighboring neuron.
2.
Action potential is a brief fluctuation in membrane potential caused by the rapid opening and
closing of the voltage–gated ion channels which is known as the spike of neuron, nerve impulse or
discharge. The action potential sweep like a wave along axons to transfer information from one
neuron to the other in the nervous system.

Neurone Function Essay
Membrane proteins are found in all cell membranes and it is these that determine the majority of the
membranes functions. There are often two types of membrane protein and these can be classified as
integral proteins and peripheral proteins. Integral proteins are situated in the hydrophobic interior
part of the phospholipid bilayer and can have hydrophilic channels that allow the passage of
hydrophilic substances across the membrane. Where as, peripheral proteins are not embedded in the
bilayer at all and are instead loosely bound to the surface of the membrane. Neurons are the basic
units of the nervous system and are involved in the transmission of impulses to all different parts of
the body. Membrane proteins are of great importance when it comes to considering the function of
neurones within the body, as many of the processes that occur would not be possible without the
action of proteins.
One of the key ways that membrane proteins are involved in neurone function is through the
formation of the resting potential. The resting potential is the charge difference across a cell
membrane when a neurone is at rest and not sending a signal, typically between –60 and –80
millivolts. Potassium and Sodium ions play a fundamental role in the formation of the resting
potential (Professor Sandidge/Moyle, 2012) and these ions each have a concentration gradient
across the membrane of a neuron. In the majority of neurones, the concentration of potassium is
greater inside the cell,

Neuroplasticity Research
The neuroplasticity term was suggested first by William James in the 19th century as a result of his
observations concerning the relationship between an animal's behavior and the brain structural
alteration. Later, based on their experiments with cats and monkeys, two neurophysiologists
concluded that plasticity is restricted by the critical period. However, recent studies contradict their
conclusion by confirming that plasticity can be extended to the duration of the whole life
experience. Thus, neuroplasticity, which is experience–dependent, is defined as an alteration in
structural and functional neural connections (Fu & Zuo, 2011). In order to understand the
mechanism of neuroplasticity, scientists have used technology to access within ... Show more
The Hebbian synapse, which means, " neurons fire together wire together", can be strengthened
when it is iteratively used because it is activity–dependent. If the agreement between pre– and
postsynaptic neurons is lasted longer, the trans–synaptic bridge can stabilize the synapse (Carvell,
2014). The morphological changes in the dendritic spines contribute to our memory and learning. To
illustrate, when the spine is small, Glutamate released by presynaptic spine activates the ionotropic
receptors, NMDA and AMPA. With many efficient depolarizations, Ca++ enters the NMDA and
AMPA in the postsynaptic spines. As a result, the spine head becomes bigger, and the spine becomes
more stable, and then it forms mushroom, which preserves long–term memory, and only AMPA
receptors will be on the membrane surface (Carvell, 2014). There are proteins that increase the
stability of the dendritic spines e.g. calcium/calmodulin dependent protein kinase II (CaMKII) and
protein kinase C (PKC) are involved in LTP maintenance and behavioral learning. In the
metabotropic receptors, cascade organizes the local protein production, whereas actin–regulatory
proteins impair LTP maintenance to modify the spine size to make it either longer or shorter. In
addition, altering the structure in postsynaptic density (PSD) enhances trans–synaptic protein
bridges, and it leads to form new spines, remove the previous spines, and it promotes the synapse
stability (Caroni et al.,

Support Of The 2016 Pathfinder Award Nomination For...
I write this in strong support of the 2016 Pathfinder Award nomination for Isabella (Bella) Greene, a
student at Oxbridge Academy of the Palm Beaches. At the outset, let me state that Bella is an
extraordinary student and it is truly a pleasure to write this letter about her.
When Bella first contacted me in 2014 expressing her interest in working in my lab, I gladly
accepted her. High School students in general are very busy with their studies, homework and
extracurricular activities. From the beginning, she committed herself to a weekly average lab work
schedule of 12–14 hours along with additional time on the weekends for the opportunity to learn
new procedures. The kind of passion and commitment Bella exhibited is truly exceptional.
My laboratory focuses on understanding the basic mechanisms of memory storage and aging
associated cognitive dysfunction and we are actively trying to develop novel therapeutics for
Alzheimer's disease. Bella is involved in a project that is aimed at elucidating the molecular
underpinnings of the establishment and maintenance of excitatory and inhibitory synapses. The
molecular mechanisms underlying this process remain elusive. Bella's goal is to determine whether
a specific family of molecular motor proteins, kinesins, plays a critical role in this process. There are
about 40 different kinesins and she wanted to identify a specific kinesin that is responsible for the
establishment and maintenance of components of excitatory and

Excitatory Synapses Research Paper
The Differences Between Excitatory And Inhibitory Synapses.
Identifying the differences between excitatory and inhibitory synapses. Explaining and exploring the
meaning of depolarization and hyperpolarization and what causes them, excitatory or inhibitory
synapses. An excitatory synapse is a synapse in which an action potential in a presynaptic neuron
that increases the probability of an action potential occurring in postsynaptic cell. Neurons form
networks through which nerve impulses travel, each neuron through which nerve impulses travel,
each neuron often making numerous connections with other cells. At an excitatory synapse, the
neurotransmitter opens sodium channels, a little depolarization of the receiving neuron occurs
because of the movement of the positively ... Show more content on Helpwriting.net ...
If depolarization of the postsynaptic membranes reaches their limit, an action potential is produced
in the postsynaptic cell.
An inhibitory synapse is a kind of synaptic potential that makes postsynaptic neurons less likely to
generate an action potential. An inhibitory
Postsynaptic potential is the change in the membrane voltage of a postsynaptic neuron, which occurs
from synaptic activation of inhibitory neurotransmitter receptors. The most common inhibitory
neurotransmitters in the nervous system are Gaba and glycine. A postsynaptic potential is considered
inhibitory when the resulting change in membrane voltages making it harder for the cell to fire an
action potential, lowering the firing rate of the neuron. Inhibitory synapses are of course the
opposite of excitatory postsynaptic potentials, which result from the flow of ions into the cell.
Inhibitory Synapses
1. The neurotransmitter at inhibitory synapses hyperpolarizes the postsynaptic membrane.
2. The GABA receptor is a ligand –gated chloride channel. The binding of GABA increases the
influx of chloride ions into the postsynaptic cell raising its membrane potential. This is extremely
fast response only taking a

Terrible Tooth Case form Essay
An Nguyen
Period 2
Physiology
The Case of the Terrible Tooth!
Part 1 ––The Dentist
Questions
1. List the symptoms experienced by Mr. Gower.
Mr. Grower experiences symptoms such as feeling hot, and light headedness, and unawareness. He
felt hot and warm prior to the root canal removal. Therefore this symptom is most likely hinting at
some problems he got before the removal. His symptoms of lightheadedness could be due to the
effects of the surgery or anesthetic. Need more information to be sure.
2. Novocain blocks action potential production at the site of injection. How do you think Novocain
works on the axon membrane, and how does it block the sensation of pain?
Novocain serves to block receptors on nerve cells that sense pain. ... Show more content on
Helpwriting.net ...
a. Which presynaptic cell must have action potentials to produce one or more action potentials in the
postsynaptic cell?
Excitatory presynaptic cell must have action potentials to produce one or more action potentials in
the postsynaptic cell because they promote depolarization of membrane which is needed to cause an
action potential. On the other hand Inhibitory presynaptic cell promote hyperpolarization which
goes against producing an action potential.
b. What phenomena must take place for the small postsynaptic potentials to reach threshold and
produce action potentials?
Summation of Excitatory postsynaptic potential and Inhibitory postsynaptic potential must take
place. More specifically spatial summation, which means that all the types of potential must add up
to be greater (less negative) than the threshold potential of –55mv for an action potential to occur in
the postsynaptic neuron.
c. If the frequency of action potentials in this presynaptic cell (#10a) increases, what happens to the
number of action potentials in the postsynaptic cell?
If the frequency of action potentials in the excitatory presynaptic cell increases than the number of
action potentials in the postsynaptic cell will increase as well. This is due to temporal summation of
EPSP at very frequent times. This causes the postsynaptic cell to produce many action potential in

succession.
d. What happens to the number of action potentials in the postsynaptic cell if the other presynaptic

The Effect of Drugs, Toxins, and Other Molecules on...
The effect of drugs, toxins, and other molecules on synapse and synapse transmission.
The synapse is the small gap separating two neurons, the presynaptic neuron (neuron that carries the
impulse to the synapse,) and postsynaptic neuron (neuron that carries the impulse away from the
synapse.) It separates the axon terminals of the presynaptic neuron from the postsynaptic neuron.
The synapse is made of three major parts: a presynaptic neuron, a postsynaptic neuron, and a
synaptic cleft. The presynaptic neuron contains the neurotransmitters, mitochondria, endoplasmic
reticulum, and other cell organelles. The postsynaptic neuron contains receptor sites for the
neurotransmitters in the presynaptic neuron. The synaptic cleft is the space ... Show more content on
Helpwriting.net ...
The series of EPSPs added together is the process of summation. If the threshold is reached, then an
action potential is generated. There is a synaptic delay within the arrival of stimuli at the presynaptic
knob and the result of the stimuli on the postsynaptic membrane. This delay is about 0.2 to 0.5
milliseconds long. The synaptic delay is a result of the increased concentration of calcium ions and
the release of the ACh.
Step 4: Acetylcholinesterase (AChE) breaks down all of the ACh in the synaptic cleft and removes it
from the postsynaptic ending. The AChE does this by hydrolyzing the ACh molecules into acetate
and choline. The presynaptic knob then absorbs the choline from the synaptic cleft. The choline
molecules are used to remake ACh. When ACh molecules are recycled, the recycling and transport
mechanisms may not be able to keep up with the neurotransmitter. This results in synaptic fatigue,
where the synapse is inactive until ACh is replenished.
Above is an explanation about the synapse and the transmission of synapse, below is the description
of the effects of drugs and toxins on synaptic transmissions. Most drugs that affect the nervous
system do so by influencing the transmission of nerve impulses across synapse. Drugs may affect
the release of the neuron transmitter; others modify the effect that the neurotransmitters have on the
postsynaptic membrane.
Medical drugs have different effects on synapses and the nervous system

Inhibitory Neurotransmitters
What are Neurotransmitters?
Neurotransmitters are various chemicals in the brain that work to convey information throughout the
brain and the rest of the body. They work to intensify electrical signals that are passed to neurons
(nerve cells). The brain holds the role of coordinating and processing complex information, and how
the brain deals with this job depends on the delicate balance of several different chemicals.
Neurotransmitters allow nerve cells to communicate messages by secreting these chemicals and
sending impulses across a synapse (the junction point between two neurons). There are many
requirements in which a molecule must meet in order to be classified as a neurotransmitter. Firstly,
the molecule must be synthesized inside ... Show more content on Helpwriting.net ...
It also regulates pleasurable emotions. Drugs such as heroin, cocaine, nicotine, and alcohol increase
the level of dopamine in the body. A drastically low level of dopamine has been linked to
Parkinson's disease, while schizophrenics are frequently found to have too much dopamine in the
frontal lobes of their brains. In addition, imbalances in this neurotransmitter have been linked to
cases of attention–deficit/hyperactivity disorder (ADHD). Serotonin is a vital inhibitory monoamine
neurotransmitter that can have strong effects on emotion, mood, awareness, and anxiety levels. It is
involved in controlling sleep, alertness, and eating. Psychedelic drugs, such as LSD, connect to the
serotonin receptor sites, and thus hinder the transmission of nerve impulses in order to change
sensory experiences. Depression, suicide, spontaneous behaviour, and hostility all appear to involve
certain discrepancies in the balance of serotonin

Essay on Neurobiological Mechanisms for Alcoholism
Neurobiological Mechanisms for Alcoholism
While alcohol could well be considered the most socially acceptable psychoactive drug in our
society, the dangers of alcohol abuse and addiction are well known. However, not everyone who
uses, or even abuses, alcohol will actually become an alcoholic who is physically dependent on the
drug. Not all of the mechanisms that cause one to become addicted to alcohol have been clarified.
However, there seem to be two main reasons for alcohol addiction. One is that the chronic
consumption of alcohol causes changes in the brain that result in a dependence on alcohol. Another
is that some individuals have abnormalities in their brains that result in a greater tendency to become
addicted to alcohol. The ... Show more content on Helpwriting.net ...
This manifests itself as increased tolerance to the effects of alcohol, since more of the drug is
required to achieve the same depressant and intoxicating effect.4 Because of the damage to the
function of the GABA inhibitory system, the CNS tends toward hyperexcitability, resulting in the
anxiety, tremors, disorientation, and hallucinations associated with alcohol withdrawal. Chronic
exposure to alcohol may also increase the sensitivity of glutamate receptors, and since glutamate is
an excitatory neurotransmitter this would contribute further to CNS hyperexcitability.5
Alcohol also seems to affect the binding properties of receptors for opioid peptides, as well as the
synthesis of these peptides. Specifically, alcohol may stimulate the release of <beta>–endorphins,
neurotransmitters held responsible for euphoria and anesthesia, accounting for some of the
intoxicating effects of alcohol.6 The experimental observation that the administration of opioid
blockers reduces craving for alcohol has led to FDA approval of naltrexone, a drug that interferes
with the function of opioid receptors, as a treatment for alcoholism.7
Thus, alcohol can cause physical addiction directly through its effects on many receptor sites in the
postsynaptic membranes of neurons. However, another important factor in the development of
alcoholism appears to be that the brains of alcoholics have abnormal neurotransmitter systems,

How The Brain Works: How Does Brain Work?
How does the brain work? Well first and foremost sex happens. We each begin as a single
microscopic cell, the fertilized egg. Within only 12 hours after fertilization, the single cell begins to
divide forming a small mass of homogeneous cells that continually divide to form the blastocyst. By
a week or so, the ICM or emerging human embryo separates into 3 distinct cell layers, the ectoderm,
the mesoderm, and the endoderm. As the cell layer thickens, it folds in on itself forming the neural
groove, a thickened collection of cells form and from the 2nd–8th week, the ridges of the neural
groove come together forming the neural tube. The neural tube is the beginning of the development
of the brain. The anterior part of the neural tube consists ... Show more content on Helpwriting.net ...
The five major divisions of the brain are the telencephalon, the diencephalon, the mesencephalon,
the metencephalon, and the myelencephalon. The telencephalon includes the cortex, basal ganglia,
and the limbic system which are responsible for performing complex cognitive processing,
voluntary movement, and in emotion and learning. The diencephalon is composed of the thalamus
and hypothalamus and these are responsible for all incoming sensory information to go to the
appropriate regions of the cortex for further processing and the hypothalamus is responsible in
regulating several vital functions by controlling the release of hormones from the pituitary gland.
The mesencephalon includes the tectum, which is composed of the inferior colliculi, and the
superior colliculi and these structures are involved with auditory and visual functions. The
metencephalon consists of the pons and the cerebellum and their main function is sensorimotor

The Chemical Structure Of Pregabalin
Introduction Pregabalin, trade name Lyrica, approved for its anticonvulsant properties and to relieve
pain in those who suffer from diabetic neuropathy. The chemical structure of pregabalin is
structurally analogous to γ–aminobutyric acid (GABA), an inhibitory neurotransmitter found in the
central nervous system and functions by binding to α2δ voltage–gated calcium ion channel in
presynaptic, inhibiting the release of neurotransmitters, most notably GABA. By decreasing the
amount of the inhibitory neurotransmitter GABA in synaptic terminals, epileptic seizures can be
controlled and prevented.1
Each drug displays its own properties when introduced to the body and all traits must be evaluated
to observe effectiveness and side effects that may occur. Pregabalin, although structurally and
functionally similar to gabapentin (trade name Neurontin), has been shown to be more potent and
exhibits linear kinetic properties, unlike gabapentin. Some factors that contribute to its success are
that it has a bioavailability of 90%, 98% is excreted in urine unchanged, thus no or few side
reactions occur, and it is able to pass through the blood–brain barrier. Beneficial effects of taking
pregabalin can be observed in as little as 2 days of administration, unlike most other central nervous
system drugs, which typically take effect.1
Pregabalin is prescribed to treat conditions such as epilepsy and diabetic neuropathy. In addition,
pregabalin has been approved for the treatment of

The Nervous System And Peripheral Nervous Systems
The nervous system has three general functions: a sensory function, an interpretative function and a
motor function. Sensory nerves gather information from inside the body and the outside
environment. The nerves then carry the information to central nervous system (CNS). Nervous
tissue consists of two main types of cells: neurons and neuroglia. Neurons also so known as nerve
cells ") transmit nerve impulses that move information around the body. Central Nervous System
and Peripheral Nervous System are Identified as the two major groups of nervous system organs
while CNS = brain & spinal cord and PNS nerves that extend from the brain (cranial nerves) and
spinal cord (spinal nerves). Sensory receptors respond to stimuli and transmit data about them to the
brain. In the skin, receptors detect touch, pressure, vibration, temperature, and pain. Elsewhere in
the body, more specialized receptors detect light (see How the eye works), sound (see The
mechanism of hearing), smell, and taste. The body nervous system detects the changes affecting the
body, make decisions, and stimulate muscles or glands to respond. The responses counteract the
effects of the changes, where the nervous system helps maintain homeostasis. Neurons vary in size
and shape and also differ in the lengths and sizes because of their axons and dendrites. A neuron has
4 basic parts: the dendrites, the cell body which is also called the soma, the axon and the axon
terminal. Dendrites – Extensions from the neuron

Autonomic Nervous System
The two divisions of the autonomic nervous system (ANS), sympathetic (SNS) and parasympathetic
(PNS), function in a complementary and integrated manner to maintain homeostasis. The output of
the autonomic nervous system is quick in comparison to the endocrine system functions. In most
cases, these systems have opposite effects, where one initiates a physiological response and the
other inhibits. The nerves of this system regulate vital internal functions which are generally
performed without conscious control (Khan Academy, 2014).
The output of the ANS effects smooth, cardiac muscle and glandular tissue (Betts et al, 2013)
The sympathetic division is associated with the "fight or flight" response, dominating in stressful
situations ... Show more content on Helpwriting.net ...
The synapse at the axon terminal of the postganglionic neuron and the target effector cell (in the
form of muscle or gland) uses epinephrine/norepinephrine (adrenaline/noradrenaline) (AK Lectures,
2014)
The parasympathetic division however, is concerned with "rest and digest" responses and when
active, reverses the effects of the SNS. The PNS system increases blood flow to digestive organs and
excretory system and decreases the blood flow to skeletal tissue (an opposite effect to the SNS) (AK
Lectures, 2014) Salivary secretion is increased and gastric motility is stimulated to facilitate
digestion (McCorry, 2007). The PNS either originates at the start of the spinal cord or at the end
(Khan Academy, 2014). The preganglionic neuron is of long structure and uses acetylcholine to
transmit signals to the shorter postganglionic neuron. The postganglionic neuron continues to use
acetylcholine to transmit to the target effector cell (AK Lectures, 2014)
Question 2 (1.3)
Using Illustrations, and a short commentary, describe the sensory and motor neuron.
Figure 1– A Motor Neuron (Biologymad, n.d.)
Figure 2– A Sensory Neuron (Biologymad, n.d.)
(200)
Sensory neurons are unipolar (Betts et al, 2013) Sensory (afferent) neurons transmit impulses from
sensory receptors to the CNS and Motor (efferent) neurons transmit impulses from the CNS to
effector muscle and

Nervous System Analysis
As we do simple actions in our life we start to do them so often that we don't even realize how and
when we are doing them. For example when we get ready to ride a bike we just get on the bike and
go, because we have done it so many times that it just comes naturally to us. Another example is
watching a scary movie and putting popcorn in our mouth at the same time. Well it is our nervous
system that helps us to do these simple actions because it handles information. When our phone
rings there are a number of functions that go on in our brain. The first thing would be our neurons in
the auditory cortex which picks up the sound of the ringing phone, neuron functions are then going
to relay the information to higher areas to process what's going ... Show more content on
Helpwriting.net ...
They supply nourishment to neurons, help remove neurons' waste products, and provide insulation
around many axons. The primary role is to shield synapses from the chatter of surrounding neuronal
activity, enhancing the signal to noise ratio in the nervous system. The Neural Impulse uses energy
to send information. The resting potential of a neuron is its stable, negative charge when the cell is
inactive An action potential is a very brief shift in a neurons electrical charge that travels along the
axon. After firing the action potential the channels in the cell membrane that opened now close up.
Some time is needed before they are ready to open and fire again. The absolute refractory period is
the minimum length of time after an action potential, during which another action potential cannot
begin. Special junctions called synapses which depend on chemical messengers. A synaptic cleft is a
microscopic gap between the terminal button of 1 neuron and the cell membrane of another neuron.
The neuron that sends a signal across the gap is called the presynaptic neuron, and the neuron that
receives the signal is called the postsynaptic neuron. The arrival of an action potential at an axon's
terminal buttons triggers the release of neurotransmitters chemicals that transmit information from 1
neuron to another. Most of these chemicals are stored in small sacs called synaptic vesicles.
Receptor sites are tuned to recognize and respond to some neurotransmitters but not to others. When
a neurotransmitter and a receptor molecule combine, reactions in the cell membrane cause a
postsynaptic potential, a voltage change at a receptor site on a postsynaptic cell membrane. They are
graded which means that they vary in size and that they increase or decrease the probability of a
neural impulse in the receiving cell in proportion to the amount of voltage change. An excitatory
PSP is a

What Is Intrinsic Excitability?
NEUR 411– Assignment 3
Ana Persson
Intrinsic excitability refers to the predisposition of a neuron to fire action potentials when exposed to
an input signal, either pre–synaptic activity or a direct input from a sensory modality (Schulz, 2006).
The intrinsic excitability of neurons is responsible for the conversion of synaptic input to the output
of a given neuron. The processes leading intrinsic excitability of neurons, also known as intrinsic
plasticity, is the constant change of a neuron's intrinsic electrical properties by neuronal or synaptic
activity (Cudmore and
Desai, 2008). This is facilitated by changes in the expression level or biophysical properties of ion
channels in the membrane, and can affect synaptic integration,
subthreshold ... Show more content on Helpwriting.net ...
Polyunsaturated fatty acids (PUFAs) have been shown to reduce neuronal sodium and calcium
currents (Nishikawa at al., 1994) and inhibit or activate potassium channels (Poling et al., 1996) and
so PUFA could be an effective anticonvulsant. The PUFA docahexanoic acid (DHA) facilitates
excitatory synaptic transmission mediated by N–methyl–D–aspartate (NMDA)–type glutamate
receptors (Nishikawa at al., 1994) and also alters inhibitory neurotransmission in some neuron types
by reducing responses to the inhibitory transmitter γ–amino–butyric acid
(GABA) (Hamano et al., 1996). A more dynamic and direct participation of DHA in the modulation
of cell signaling has been reported in interaction with and blockage of neuronal voltage–gated
potassium channels (Poling et al., 1996). It is probable that PUFA effects are locally specific and
may vary according to developmental stage. In cardiac myocytes, long–chain PUFAs inhibit
voltage–dependent sodium channels and L–type calcium channels, thus stabilizing the membrane. It
was shown that long–chain PUFAs produce a transient elevation of seizure threshold in a cortical
stimulation model

Aggression And Its Effects On Human Behavior Essay
Aggression plays a significant role in the survival of many organisms. Studies have shown that
aggression may be an evolved behavior to overcome certain adaptive problems (Buss & Duntley,
2006; Buss & Shackelford, 1997). Aggression is often used to acquire resources, protect mates and
offspring, and to warn off predators and to hunt prey. Even though, aggression has proved to be
useful for the survival of many organisms it is still a costly behavior to express. Aggression can
often result in the injury or death of organisms that use this behavior. Due to the high risks
associated with aggressive behaviors, it is possible the brain may have evolved certain mechanisms
to control the expression of this behavior (Wong et al., 2016). There have been many studies
conducted that suggest the hypothalamus or the lateral septum (LS) are involved in the suppression
of aggression (Bard, 1928; Potegal, Blau, & Glusman, 1981; Lee & Gammie, 2009). Bard (1928)
conducted a series of experiments that involved the removal of different areas of the diencephalon
(area above the brain stem) of cats. The diencephalon is an area of the brain that contains the
hypothalamus (Bard, 1928). Bard (1928) presented evidence that the removal of the diencephalon
from the cranial to the middle and the removal of the dorsal part of the thalamus elicited a hostile
response from the subjects. Moreover, in the 1980's, it was shown that the stimulation of the septal
region inhibited intraspecific aggression

Sympathetic Noradrenergic System Research Paper
The sympathetic noradrenergic system plays major roles in tonic and reflexive changes in
cardiovascular tone. Adrenaline is a major determinant of responses to metabolic or global
challenges to homeostasis. Adrenaline responses to stressors are more closely linked to responses of
the hypothalamic‐pituitary‐adrenocortical system than of the sympathetic nervous system. The
sympathetic noradrenergic system is active even when the individual is at rest and maintains tonic
levels of cardiovascular performance. Adreno receptors in the membranes of effector cells determine
the physiological and metabolic effects of catecholamine. Beta‐adrenoceptors mediate stimulatory
effects of catecholamine on the rate and force of the heartbeat; stimulation of ... Show more content
on Helpwriting.net ...
1) Once action potential reach to the presynaptic terminal.
2) Depolarization of presynaptic terminal will open the Calcium ion channels and Calcium ions
diffuse into the axon terminal.
3) Synaptic vesicles fuse with membrane and open, Ca2+ triggers the release of Neurotransmitter
from vesicles.
4) Neurotransmitter diffuses across the synaptic cleft and binds to the receptor sites of postsynaptic

Protocols For Training For The Different Learning Paradigms
Protocols for training for the different learning paradigms are shown in Fig 1. We anticipate that we
will observe aging–dependent decrease in the ability to learn as reported in vertebrates. In order to
understand synaptic aging, the above behavioral experiments will be coupled with
electrophysiological measurements of L7MN–LESN connections. Briefly, in the above preparation,
abdominal ganglion is partially desheathed to gain access to measure electrophysiological properties
using sharp electrodes. Similar experiments were performed on R15 neuron in the abdominal
ganglia (See Fig 2&3). Specifically, we will measure the resting membrane potential, and resistance
and postsynaptic potentials (PSPs) before and after different behavior training paradigms described
above [6,34]. PSPs are a measure of strength of synaptic connections. These experiments will
answer whether during aging (1) passive properties such as basic membrane resting potential and
resistance change and (2) active properties such as excitatory and inhibitory PSPs change.
How does aging affect synaptic plasticity? (Aim1) We will carry out synaptic plasticity
measurements using a reduced preparation containing abdominal ganglia from mature and old
animals. Specifically, we will expose the abdominal ganglion to plasticity–inducing regimens of 5–
HT stimulation examining intermediate–term facilitation ( Jin et al., 2012a,b; Sutton and Carew,
2000; Ghirardi et al., 1995) and LTF. These experiments would provide

Identify And Explain The Difference Between Voluntary And...
Every day, our body naturally responds to environmental stimuli by one of two mechanisms, a
voluntary reaction or an involuntary reflex. The nerves and muscles work together to respond to a
change in the body's environment, both internal and external, with the intent of maintaining a
homeostatic state. Common reflexes include slipping and righting oneself, as well as immediately
and naturally withdrawing a body part that made contact with a hot object. A reflex typically occurs
prior to the brain fully processing the information regarding the stimulus. Conversely, a voluntary
action is controllable and learned by experience (G). The most well
known learned response is
Pavlov's dogs, who were shown to salivate at the ring of a bell because it signaled food was coming.
Both voluntary and involuntary responses go through neural pathways beginning with a receptor
that receives a stimulus from the environment. This stimulus elicits an action potential, which
carries ... Show more content on Helpwriting.net ...
Many factors, including receptor function, neuron stimulation, length/complexity of neuronal
pathway, difference between sensory/motor neuron conduction velocities and synaptic transmission,
influence the reaction time. Of utmost importance is the synaptic transmission, which refers to how
presynaptic cells communicate with postsynaptic cells by releasing neurotransmitters which, when
collected at the postsynaptic cells receptors, work to engage a response. This process has the
potential to be altered for any duration of time by either improving or impairing its potential.
Postsynaptic neurons receive both excitatory and inhibitory inputs, which have the capability to
increase or decrease the likelihood of the nerve firing an action potential. Both types of input are
being applied to the receptor at all times while

Essay Comparing The Cartesian Model And Specificity Theory...
Many theories have been suggested for clinical presentation of pain such as Cartesian module of
pain in the 17th century and the 19th century specificity theory of pain. The 20th century central
summation, sensory interaction, gate control, and biopsychosocial theories show deferent concepts
from the simpler cause and effect approaches that essential in the Cartesian model and specificity
theory. Traditionally within physiotherapy and medicine the medical/disease model has been
suggested. Medical/Disease model acts on the basis that all pain has a dominant tissue or structural
source. This model is founded on the Cartesian model and specificity theory of pain where pain is
considered as sign of tissue injury and damage (Waddell, 2004)
Currently, it has bee classified the pain based on the underlying neurophysiological mechanisms
responsible for its generation and/or maintenance. The mechanisms based classification for pain is
essential for physiotherapists to better understand of clinical presentation of pain and can improve
the clinical outcomes by directing treatment into the dominant neurophysiological mechanisms
underlying the pain (Smart et al, 2008). ... Show more content on Helpwriting.net ...
In case of tissue injury, pain occurs immediately results of local release of chemicals that act on the
nerve terminal. Dorsal horn cells (substantia gelatinosa) are mainly short inhibitory interneurons and
regulate transmission at the first synapse of the nociceptive pathway, between the primary afferent
fibers and the spinothalamic tract transmission neurons. Inhibitory interneurons are activated by
descending inhibitory neurons or by non–nociceptive afferent input. This gatekeeper function
support the gate control theory (Raina et al,

pain Essay
Q.2– Discuss what neuromodulators are and how they modulate the sensation of pain.
The sensation and clarification of pain includes activation of individuals brain regions associated
with spatial discriminative and affecting mechanisms of pain awareness. This is clearly a potential
concern of movement of the primary afferent nociceptor, and comprises integration of the
polysynaptic yield from the primary afferent through several arising pathways. The exact position of
specific supraspinal regions related with pain perception is complex and rather unstated. Present
research has focused on spinal mechanisms of pain transduction.
The dorsal horn comprises of multiple peptide and amino acid neurotransmitters, neuromodulators,
and ... Show more content on Helpwriting.net ...
Nociceptors have a major role in pain pathway. As shown in the diagram above Aδ and C fibres are
the free nerves ending by which the nociceptors are established to be the primary afferent fibers,
every fiber have diverse features in terms of myelin sheets, diameter and thresholds to control the
speed of the signal to reach the secondary afferent neurones . Next, the synapse of the dorsal horn of
the spinal cord receives the signal from Aδ and C fibres that sends information to the nociceptive
specific neurons located in rexed lamina I and II resulting of secretion of excitatory
neurotransmitters like substance P and glutamate. Moreover, complex interactions are involved at
the level of dorsal horn between afferent neurons by which they determine the function of the
secondary afferent fibers in terms of excitatory or inhibitory. Furthermore, mainly there are two
pathways that a signal can reach the brain through.
The spinothalamic tract which involves 2nd afferent neurons that decussate within the segments of
the level of entry of the spinal cord raising the contralateral spinothalamic tract to reach the
thalamus and then third afferent fibers carry the signal to the somatosensory cortex in the brain, such
pass way is to localization of the pain The spinothalamic tract is when the nerve fibers also
decussate in the spinal cord but they project to brainstem reticular formation before reaching the
thalamus. Other than that, there so many projection to the

Epilepsy Is A Central Nervous System Disorder ( Cns )
Introduction
Epilepsy is a central nervous system disorder(CNS) causing recurrent seizures and can only be
defined when there is at least one epileptic seizure.[1][2] John Hughlings Jackson, a notable British
neurologist proposed that epilepsy is "an occasional, an excessive and a disorderly discharge of
nervous tissue". About 65 million people(1% of the human population) in the world have epilepsy
and the cases account for 80% in developing countries. [3][4] In this essay, the normal physiology of
nerve transmission in cerebral cortex and pathophysiology of epilepsy will be discussed. The
mechanism of action of valproate is also studied and how it leads to the treatment of epilepsy.
Normal Physiology of Nerve Tranmission in Cerebral Cortex
The body system that is affected by epilepsy is CNS which is consisted of the brain and the spinal
cord.[5] (Figure 1) Figure 1 The major divsions of CNS[5]
The brain has a part called the cerebral cortex(gray matter) which is made up of 3 to 6 layers of
neurons.[7] A neuron has three parts namely axon, dendrites and cell body.[6] Neurons are classified
as principal(projection) neurons and interneurons. Principal neurons transmit information to other
neurons in the brain and form excitatory synapses. Interneurons in the CNS transmit impulses
locally and form inhibitory synapse.[7] Two common types of pathways for these neurons include
recurrent feedback pathways and feed–forward pathways.[9](Figure 2) `

Synthesis Of Basal Ganglia
In terms of motor control, the basal ganglia is composed of interconnected nuclei located in the
telencephalon, diencephalon, and midbrain which include the striatum, globus pallidus (GP),
entopeduncular nucleus (globus pallidus internal in humans), subthalamic nucleus, and the
substantia nigra (figure1) (6,8). Although there are multiple structures that partake in the modulation
of movement, the basal ganglia serves to integrate information deriving from the parietal, frontal,
and temporal cortex. In particular, electrical stimulation from the cortex to the striatum derive from
regions implicated in the planning and execution of motor movement (6). All of this information
converges and activates GABAergic medium spiny neurons (9). Of note, ... Show more content on
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It has been demonstrated that altered activity of pallidal neurons evoke irregular signaling patterns
of dopaminergic neurons, which in turn may cause a shift in signaling rates to the stiatum and its
activating role of the indirect pathway (7). Interestingly, axonal collaterals from the substantia nigra
pars compacta also provide innervation to the globus pallidus through dopaminergic signaling
(5,1,13). The literature suggests that activation of dopamionergic receptors in the globus pallidus
play an important regulatory role of GABAergic activity. Therefore, stimulation of dopaminergic
receptors is also involved in the modulation of pallidal firing. The depletion of dopaminergic
stimulation in the pallidus suggests a potential role in PD motor deficits and correlation with
symptoms such as tremors and dyskenisia (1,2) .Interestingly, experiments conducted in non–human
primates have demonstrated that a decrease in dopaminergic inputs to the globus pallidus, due to
degeneration of dopaminergic neurons in the substantia nigra pars compacta, triggered irregular
firing patterns (1,4); however, the precise role of these dopaminergic projections that cross and
directly innervate the GP in parkinsonian physiopathology is not clear

Part of the Neuron Affected, Inhibitory or Excitatory...
Part of the Neuron Affected, Inhibitory or Excitatory Potential
Changes and Ion Channels Affected by Psilocybin
Psilocybin belongs to the classification of drugs called hallucinogens. Hallucinogens typically act by
stimulating serotonin receptors at different times or for longer durations than serotonin itself would
(Kalat 2004). When psilocybin enters the brain, the enzyme alkaline breaks down one of its
phosphate groups through hydrolysis. It then becomes psilocin, an even stronger hallucinogen
(Psilocybin 2003). It is particularly potent due to the position of its hydroxyl group (Jacobs 1984).
Psilocin is a postsynaptic serotonin receptor agonist. In other words, its similar structure allows it to
mimic ... Show more content on Helpwriting.net ...
The other is to suppress sensory systems during the waking state
(Powell 2004). When psilocin binds to the 5HT2A receptors, it inhibits the uptake of serotonin,
thereby decreasing inhibitory serotonin activity. This results in an increase of alertness and arousal.
Another theory asserts that the important activity of psilocin takes place at the proximal dendrites of
level V pyramidal cells, as this is the area of the brain with the highest concentration of 5HT2A
receptors. In support of this theory, this is the only area of the brain where directly applies serotonin
excites cells. The receptors do not activate pyramidal cells directly but through action potential. This
is demonstrated by the fact that drugs that stop the action potential prevent the 5HT2A induced
excitation. While action potential is required for such excitation, stimulation of the
5HT2A receptors does not result in increased action potential.
The excitation mechanism can also be blocked by presynaptic inhibitors, showing that activity in the
presynaptic 5HT2A receptors that connect with pyramidal cells is also crucial
(Connely 2004). According to Marek and Aghajanian 1998, page
1123, "An enhancement of asynchronous evoked [excitatory postsynaptic potentials] via 5HT2A
receptors provides a possible synaptic mechanism for the hallucinogenic effects of these drugs."
Psilocybin is an indoleamine, in the same chemical group with serotonin and

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