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Multi-photon Intracellular Sodium Imaging Combined with UV-mediated Focal Uncaging of Glutamate in CA1 Pyramidal Neurons
Published on: October 8, 2014
L-type calcium channels modulate glutamate-driven bursting activity in the nucleus accumbens in vivo
1Department of Neuroscience, Finch University of Health Sciences, The Chicago Medical School, 3333 Green Bay Rd, North Chicago, IL 60064, USA.
Abstract:
The majority of adult nucleus accumbens medium spiny neurons exhibit a bistable membrane potential that fluctuates between a relatively hyperpolarized (Down) state (average=-76 mV) and a less hyperpolarized (Up) state (average=-60 mV) near firing threshold. During in vivo extracellular recordings from nucleus accumbens neurons, we used microiontophoresis to apply glutamate and selected neurons that fired in bursting patterns reflecting a subthreshold bistable membrane potential. The average frequency of bursts events was 0.85 Hz. The average burst duration was 392+/-3.5 ms, with an average of 13.4 spikes and an average spike frequency of 30.6+/-3.1 Hz per burst. To determine the involvement of the L-type calcium channel in the bursting pattern, we applied the benzothiazepine L-type calcium channel blocker, diltiazem. Diltiazem rapidly (<2 min) and reversibly decreased the burst duration by 29% and the frequency of spikes within a burst by 30% without changing the overall burst event frequency. The results provide the first in vivo electrophysiological evidence implicating an L-type calcium channel that modulates glutamate-induced burst firing of nucleus accumbens neurons.
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