I am pleased to invite you to attend the MiNDS Colloquium TODAY Thursday January 15th at 3:30 in HSC 4E20. Bring your coffee cup for coffee and cookies before the talk at 3:00.

Dr. Sheena Josselyn is a Senior Scientist at The Hospital for Sick Children (SickKids) and an Associate Professor at the University of Toronto.  She holds a Canada Research Chair in Molecular and Cellular Cognition.  Sheena received a PhD from the University of Toronto and conducted post-doctoral work with Mike Davis (Yale) and Alcino Silva (UCLA).  Her research is dedicated to understanding the molecular, cellular and circuit processes underlying how the brain encodes, stores and uses information.

The research in Dr. Josselyn's laboratory is dedicated to understanding the neural basis of cognitive function and dysfunction. To unravel the molecular, cellular and circuit processes that underlie learning and memory they employ a multidisciplinary approach including the use of transgenic mice, gene deletion 'knockout' mutants, and 'knock in' mutants which carry a specific point mutation, biochemistry, pharmacology, neuroanatomical lesions and detailed behavioral analysis. The guiding rationale behind this work is the finding that long-term memory (LTM) involves structural re-modeling of synaptic connections and consequently, requires gene expression and de novo protein synthesis.

Sheena's talk will discuss how a fundamental goal of neuroscience is to understand how information is encoded and stored in the brain. The physical or functional representation of a memory (the memory trace or "engram") is thought to be sparsely encoded over a distributed memory network. However, identifying the precise neurons which make up a memory trace has challenged for scientists since Karl Lashley's "search for the engram" in the 1950's (Lashley, 1950; Josselyn, 2010).  Moreover, it was not known why one neuron (rather than its neighbour) was involved in a given memory trace. Dr Josselyn's lab previously showed that lateral amygdala (LA) neurons with increased levels of the transcription factor CREB (cAMP/Ca++ Responsive Element Binding protein), are preferentially activated by fear memory expression, suggesting they are selectively recruited into the memory trace (Han et al., 2007).  Sheena, and others, went on to show that these neurons were critical components of the memory network by selectively ablating (Han et al., 2009) or inactivating them (Zhou et al., 2009).  These findings established a causal link between a specific neuronal subpopulation and memory expression, thereby identifying critical neurons within the memory trace. Furthermore, these results suggest that at least within the LA, eligible neurons compete for inclusion in a memory trace, and that the winners of this competition are determined by relative CREB function.  Although competition between neurons, axons and synapses is necessary for refining neural circuits in development, little is known about competition between neurons in the adult brain. Their recent results suggest that this neuronal competition during memory formation limits the overall size of the memory trace (number of "winning" neurons) and is a mechanism that links (or disambiguates) related memories in the LA.

            Memory impairments are a hallmark of aging, major mental illnesses (e.g., schizophrenia and depression) as well as neurological disorders (e.g., Alzheimer's and Parkinson's diseases). Therefore, understanding how the brain encodes and stores information is highly relevant to both mental health and mental illness.

We look forward to seeing you all at the talk today.

Regards

Sandra

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Kathryn M Murphy PhD

Hamilton ON L8S 4K1