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Vol. 301, Issue 3, 1119-1125, June 2002
Department of Cellular and Molecular Pharmacology, Finch University
of Health Sciences, The Chicago Medical School, North Chicago, Illinois
Dopamine D1 receptors within the nucleus accumbens (NAc) are
intricately involved in the rewarding effects of cocaine and in
withdrawal symptoms after cessation of repeated cocaine administration. These receptors couple to a variety of ion channels to modulate neuronal excitability. Using whole-cell recordings from dissociated adult rat NAc medium spiny neurons (MSNs), we show that, as in dorsal
striatal MSNs, D1 receptor stimulation suppresses N- and P/Q-type
Ca2+ currents (ICa) by
activating a cAMP/protein kinase A/protein phosphatase (PP)
signaling system, presumably leading to channel dephosphorylation. We
also report that during withdrawal from repeated cocaine
administration, basal ICa density is
decreased by 30%. Pharmacological isolation of specific
ICa components indicates that N- and R-type,
but not P/Q- or L-type, currents are significantly reduced by repeated
cocaine treatment. Inhibiting PP activity with okadaic acid enhances
ICa in cocaine withdrawn, but not control, NAc neurons, suggesting an increase in constitutive PP activity. This
suggestion was supported by a significant decrease in the ability of D1
receptor stimulation and direct activation of cAMP signaling to
suppress ICa in cocaine-withdrawn NAc
neurons. Chronic cocaine-induced reduction of
ICa in NAc MSNs will globally impact Ca2+-dependent processes, including synaptic plasticity,
transmitter release, and intracellular signaling cascades that regulate
membrane excitability. Along with our previously reported reduction in whole-cell Na+ currents during cocaine withdrawal, these
findings further emphasize the important role of whole-cell plasticity
in reducing information processing during cocaine withdrawal.
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