The way in which sensory experience is captured and converted into long lasting changes in the brain is critical for adaptive behaviors. A deficit in sensory information processing is a pronounced feature shared by many devastating neuropsychiatric disorders such autism, schizophrenia and depression. Each experience activates a unique set of neurons within specific regions of the brain. While we now know in many cases the brain regions that are associated with particular types of sensory experience, we know very little about the identity of specific ensembles of neurons that are responsible for the encoding of specific sensory information, let alone the underlying molecular and cellular mechanisms. The goal of this proposed study is to fill this gap in our knowledge by developing a versatile system that allows for the identification and manipulation of ensembles of neurons as they participate in the processing of the influx of sensory information. Using this system, our long term goal is to explore the cellular and molecular mechanisms by which sensory experience is coupled to modification of the synaptic properties of neural networks and to understand how disruption of this process leads to cognitive deficits.
The research described in this proposal will allow us to understand how sensory experience is captured and stored in the brain at the cellular and synaptic level. A deficit in sensory information processing is often implicated in devastating neurological disorders such as autism, schizophrenia, and depression, which often involve profound psychiatric and cognitive deficits in afflicted individuals. Our proposed study will shed light on the pathology and etiology of these neurological diseases.
|Weng, Feng-Ju; Garcia, Rodrigo I; Lutzu, Stefano et al. (2018) Npas4 Is a Critical Regulator of Learning-Induced Plasticity at Mossy Fiber-CA3 Synapses during Contextual Memory Formation. Neuron 97:1137-1152.e5|