Annotated bibliography final 13 n.r.e
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1. The document summarizes three research papers on the effects of nanoparticles, memory tests in mice, and axonal transport deficits. 2. One study found that intracellular gold nanoparticles can increase neuronal excitability and aggravate seizures. Another developed an automated maze to assess hippocampus-dependent memory without human interference. 3. The third study used MRI to show age-dependent axonal transport deficits in a mouse model of tauopathy, linking the deficits to hyperphosphorylated tau protein in the brain.
Annotated bibliography final 13 n.r.e
- 1. Roll Book.# 1 3 Name: Nicole S.Rivera Espinal Date:12/10/2014 Annotated Bibliography 1 Jung S, Bang M, Kim BS, Lee S, Kotov NA, Bongsoo K, Daejong J. 2014 Intracellular Gold Nanoparticles Increase Neuronal Excitability and Aggravate Seizure Activity in the Mouse Brain. PLoS ONE 9(3): e91360. doi:10.1371/journal.pone.0091360 This research paper analyzes the physiological and pathological functions of gold nano-particles (AuNPs). These particles show inert characteristics making them candidates for carrying therapeutic substances. The only problem is that the reaction of the AuNPs on the electrophysiological activity of neurons has not been examined. Because of that, their investigation is centered on the effects of intracellular application of AuNPs on the action of an individual neuron. In this experiment, AuNPs were intracellular enforced to hippocampal CA1 neurons from the rodent brain. The electrophysiological substances of CA1 neurons treated with 5- or 40-nm AuNPs was determined using patch-clap. Testing slices of hippocampal CA1 in mouse brain, researchers demonstrated that intracellular AuNPs makes hippocampal CA1 neurons become more susceptible to action potentials. Furthermore, this experiment showed that this could lead to disorders and pathological conditions. This research contributes to the understanding and application of this new technology in nano-medicine. It provides a perspective of neuronal activity variation to different substances that could complement my review paper. Annotated Bibliography 2 Pioli EY, Gaskill BN, Gilmour G, Tricklebank MD, Dix SL, Bannerman D, Garner JP. 2014. An automated maze task for assessing hippocampus-sensitive memory in mice. Behavioural Brain Research 261: 249–257.DOI: 10.1016/j.bbr.2013.12.009 The research of (Pioli et al. 2014) illustrates hippocampal disorder with memory deficiency. To study the hippocampal action of mice, researchers used a T-maze. A T-maze is generally used to assess rodent behavior in situations of rewarded alternations. A worry associated with maze protocols is that human intervention in the process alters the adequate status of the rodent. Regular mice have instinctively huge levels of alternation, whereas hippocampal-lesioned mice are dramatically damaged. To solve this problem they create an automated modular mice device controlled via computer. Rodents that underwent the new mechanism showed significantly higher performance than HPC-lesioned mice. Results showed that by reducing human contact and obtaining more stable performance the automated maze can decrease nonessential experimental disparity and increase reliability. This project contributes to the scientific community, because the automated reward system keeps the investigators from interfering with the test subjects and helps study them in a more stable environment. In addition, it provides my review paper great background information about different stimuli on the hippocampus.
- 2. Annotated Bibliography 3 Majid T, Ali YO, Venkitaramani DV, Jang MK, Lu HC, Pautler PG. 2014. In vivo axonal transport deficits in a mouse model of fronto-temporal dementia. Behavioural Brain Research 261: 249–2577. DOI: 10.1016/j.nicl.2014.02.005 Majid et al. (2014) explains how Axoplasmic transport is crucial for neurons and the deficiencies in this mechanism that have been found in some mouse models of Alzheimer disease. However, it is yet to be decided whether or not the Axoplasmic transport is deficient preceding the onsets of neurodegenerations. For this reason, they decided to use the rTg4510, which is a versatile tauopathy rodent model. This exemplary mouse shows how neurodegeneration in the forebrain is associated with behavioral deficits and Tau pathology, which is seen only as accumulation of abnormal hyperphosphorylated protein. To study the axoplasmic transport in mice, Magnetic Resonance Imaging (MRI) was induced as part of the progression of the axonal transport, then, was imaged using Manganese Enhanced Magnetic Resonance Imaging (MEMRI), each cycle was held using Paravision software. The pictures showed the presence of age-dependent axonal transport deficits starting at 3 months of age in rTg4510 mice; they associated these deficits to the hyperphosphorylated tau in the brain. This investigation contributes a model that can be used for future therapeutic interventions and provides details on how the axoplasmic transport is affected by the age of the organisms and neurons.