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Julie Robillard


 

 

 

Julie Robillard

  • B.Sc. Microbiology and Immunology, Universite de Montreal, 2003


Department: Neuroscience

Lab phone: 604-822-7893

Research Description:

The aging process and Alzheimer's disease (AD) result in similarchanges in the brain such as decreases in synaptic plasticity and memorydeficits. It is well established that hippocampal long-term potentiation(LTP), a cellular model of learning and memory, is impaired in aged mice andin mice models of AD. However, further work is needed to detail how andthrough what mechanisms synaptic plasticity is affected in aging and AD. Myproject is to characterize the synaptic plasticity deficits observed in agedmice and in a mouse model of AD using electrophysiology andimmunohistochemistry. The objectives of my project are: 1) Characterize thefrequency-dependency of hippocampal synaptic plasticity in aged mice. Whilemany studies have looked at synaptic plasticity in aged rats, the effects ofaging on hippocampal plasticity remain elusive in mice. With the risingpopularity of mice models, it is necessary to detail how aging affects themouse hippocampus. 2) Assess t he contribution of L-type calcium channelsto synaptic plasticity in aged mice and a mouse model of AD. Both aging andAD are characterized by significant calcium dysregulation in pyramidalneurons due to an increase in L-type calcium channel activity. Sincevoltage-dependent calcium channels (VDCCs) can mediate a form of LTP, Ipropose that this VDCC-LTP is increased in aged mice and in our AD model. 3)Characterize the involvement of adenosine to synaptic plasticity deficits inour models. Recent evidence suggests that adenosine, a glial transmitter,plays a role in age-related LTP deficits. Furthermore, adenosine receptorsare known to interact with L-type calcium channels. Since very little isknown about how glial cells modulate synaptic plasticity, investigatingadenosine in the context of aging and AD may provide key insights on howhippocampal synaptic plasticity is regulated.





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