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J Neurophysiol 86: 586-595, 2001;
0022-3077/01 $5.00
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The Journal of Neurophysiology Vol. 86 No. 2 August 2001, pp. 586-595
Copyright ©2001 by the American Physiological Society

Multiple Effects of Dopamine on Layer V Pyramidal Cell Excitability in Rat Prefrontal Cortex

Allan T. Gulledge and David B. Jaffe

Division of Life Sciences, University of Texas at San Antonio, San Antonio, Texas 78249

Gulledge, Allan T. and David B. Jaffe. Multiple Effects of Dopamine on Layer V Pyramidal Cell Excitability in Rat Prefrontal Cortex. J. Neurophysiol. 86: 586-595, 2001. The mechanisms underlying the inhibitory effects of dopamine (DA) on layer V pyramidal neuron excitability in the prelimbic region of the rat medial prefrontal cortex were investigated. Under control conditions, DA depressed both action potential generation (driven by somatic current injection) and input resistance (RN). The presence of GABAA receptor antagonists blocked DA-induced depression of action potential generation and revealed a delayed increase in excitability that persisted for the duration of experimental recording, up to 20 min following the washout of DA. In contrast to spike generation, disinhibition did not affect the transient depression of RN produced by DA, suggesting independent actions of DA on spike generation and RN. Consistent with the hypothesis that DA acts to decrease pyramidal cell output via a GABAergic mechanism, DA increased the frequency of spontaneous inhibitory postsynaptic currents in both the absence and presence of TTX. Furthermore focal application of GABA to a perisomatic region mimicked the inhibitory effect of DA on spike production without affecting RN. Focal application of bicuculline to the same location reversed the inhibitory effect of bath-applied DA on spike generation, while again having no effect on RN. The depression of RN by DA was both occluded and mimicked by the Na+ channel blocker TTX, suggesting the involvement of a Na+ conductance in reducing pyramidal cell RN during the acute presence of DA. Together these data demonstrate that the acute presence of DA decreases pyramidal neuron excitability by two independent mechanisms. At the same time DA triggers a delayed and longer-lasting increase in excitability that is partially masked by synaptic inhibition.




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