This document contains three annotated bibliographies summarizing research articles: The first summarizes a study finding that intracellular gold nanoparticles increase neuronal excitability and seizure activity in mice brains. The second describes research using an automated maze to assess hippocampus-sensitive memory in mice. The third summarizes a study using magnetic resonance imaging to find age-dependent axonal transport deficits in a mouse model of frontotemporal dementia.

1. Nicole S.Rivera Espinal 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.