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The Journal of Neuroscience, September 29, 2004, 24(39):8621-8628; doi:10.1523/JNEUROSCI.3280-04.2004

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Cellular/Molecular
Dopamine Excites Nucleus Accumbens Neurons through the Differential Modulation of Glutamate and GABA Release

Gregory O. Hjelmstad

Department of Neurology, Wheeler Center for the Neurobiology of Addiction and the Ernest Gallo Clinic and Research Center, University of California San Francisco, Emeryville, California 94608

Afferent activity into the nucleus accumbens (NAc) occurs in bursts of action potentials. However, it is unclear how synapses in this nucleus respond to such bursts, or how these responses are altered by dopamine (DA). I examined the effects of DA on excitatory and inhibitory responses to trains of stimuli in rat NAc slices. Both EPSCs and IPSCs showed use-dependent depression during trains. Although DA inhibited both glutamate and GABA release in the NAc, it differentially inhibited release during trains. The inhibition of IPSCs persisted throughout the train of stimuli, whereas the inhibition of EPSCs progressively diminished. This differential modulation may be explained by a calcium-dependent change in the recovery from depression at the GABA synapses, where DA acts by decreasing Ca²⁺ entry. Thus, at later stages of sustained stimulation, DA preferentially inhibits GABA release, producing a net excitatory effect during bursts suggesting a mechanism for enhancing the contrast between competing inputs into the NAc, as well as for affecting long-term plasticity in this structure.

Key words: accumbens; dopamine; depression; burst; presynaptic; calcium

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Received June 9, 2004; revised August 24, 2004; accepted August 24, 2004.

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