L-type calcium channels modulate glutamate-driven bursting activity in the nucleus accumbens in vivo.

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.