PhD candidate, Surmeier Lab, Department of Neuroscience.
The axons of striatal spiny projection neurons (SPNs) have recurrent collateral branches that target neighboring striatal neurons, including other SPNs. These recurrent collaterals provide a means of rapid local communication and figure prominently in theories of the spatiotemporal pattern of SPN ensemble activity essential for striatal functions in goal-directed movement and a range of cognitive functions, such as reward processing and decision-making. However, there are fundamental questions about the functional properties of collateral synapses that remain unanswered, making assertions about their circuit-level roles speculative. Importantly, in rodent models of Parkinson's disease (PD), the strength of recurrent collateral synapses is dramatically reduced, paralleling disruptions in ensemble architecture and motor deficits. The mechanisms that modulate SPN collateral synapses, as well as those underlying the downregulation of functional connectivity in PD, remain unclear. Ongoing work aims to rigorously characterize SPN collateral function within the striatal circuit and identify the mechanisms driving this functional suppression in PD models. To this end, a battery of cutting-edge complementary optical, electrophysiological, optogenetic, and anatomical approaches will be used to characterize the physiological and anatomical properties underlying SPN collateral connectivity, the pathways that modulate these synapses, and the factors that drive their attenuation in PD models.
Jenna Ward
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