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.

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.