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SCSB Colloquium Series: Memory, learning to learn, coordinated and discoordinated control of cognitive representations
March 1 | 4:00 pm - 5:00 pm
Speaker: André Fenton, Ph.D.
Affiliation: Professor, and Director, Center for Neural Science, New York University
Host: Dr. Matthew Wilson
Talk title: Memory, learning to learn, coordinated and discoordinated control of cognitive representations
Abstract: Biological neural networks can represent information in the collective action potential discharge of neurons, and store that information amongst the synaptic connections between the neurons that both comprise the network and govern its function. The strength and organization of synaptic connections adjust during learning, but many cognitive neural systems are multifunctional, making it unclear how continuous activity alternates between the transient and discrete cognitive functions like encoding current information and recollecting past information, without changing the connections amongst the neurons. This lecture will summarize our investigations of mutant mice that model the genetic defect in Fragile X syndrome (FXS), the most common genetic cause of autism and intellectual disability. I then describe our investigations of the molecular and biochemical mechanisms that change synaptic function to persistently store spatial memory in the rodent hippocampus. I will then report on how entorhinal cortex-hippocampus circuit function changes during cognitive training that creates memory, as well as learning to learn in mice. I will describe how the hippocampus system operates like a competitive winner-take-all network, that, based on the dominance of its current inputs, self organizes into either the encoding or recollection information processing modes. We find no evidence that distinct cells are dedicated to those two distinct functions, rather activation of the hippocampus information processing mode is controlled by a subset of dentate spike events within the network of learning-modified, entorhinal-hippocampus excitatory and inhibitory synapses. I will close by reexamining the findings from the FXS mutant mouse.