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J Neurophysiol 84: 75-87, 2000;
0022-3077/00 $5.00
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The Journal of Neurophysiology Vol. 84 No. 1 July 2000, pp. 75-87
Copyright ©2000 by the American Physiological Society

Dopamine D1/D5 Receptor Activation Modulates a Persistent Sodium Current in Rat Prefrontal Cortical Neurons In Vitro

Natalia A. Gorelova1 and Charles R. Yang2

 1Department of Psychology, University of British Columbia, Vancouver, British Columbia V6T 1Z4, Canada; and  2Neuroscience Research, Eli Lilly Co., Indianapolis, Indiana 46285-0510

Gorelova, Natalia A. and Charles R. Yang. Dopamine D1/D5 Receptor Activation Modulates a Persistent Sodium Current in Rat Prefrontal Cortical Neurons In Vitro. J. Neurophysiol. 84: 75-87, 2000. The effects of dopamine (DA) on a persistent Na+ current (INaP) in layer V-VI prefrontal cortical (PFC) pyramidal cells were studied using whole cell voltage-clamp recordings in rat PFC slices. After blocking K+ and Ca 2+ currents, a tetrodotoxin-sensitive INaP was activated by slow depolarizing voltage ramps or voltage steps. DA modulated the INaP in a voltage-dependent manner: increased amplitude of INaP at potentials more negative than -40 mV, but decreased at more positive potentials. DA also slowed the inactivation process of INaP. The D1/D5 dopamine receptor agonists SKF 38393, SKF 81297, and dihydrexidine (3-10 µM), but not the dopamine D2/D3 receptor agonist qiunpirole (1-20 µM), mimicked the effects of DA on INaP. Modulation of INaP by D1/D5 agonists was blocked by the D1/D5 antagonist SCH23390. Bath application of specific protein kinase C inhibitor, chelerhythrine, or inclusion of the specific protein kinase C inhibiting peptide[19-36] in the recording pipette, but not protein kinase A inhibiting peptide[5-24], blocked the effect of D1/D5 agonists on INaP. In current-clamp recordings, D1/D5 receptors activation enhanced the excitability of cortical pyramidal cells. Application of the D1/D5 agonist SKF 81297 induced a long-lasting decrease in the first spike latency in response to depolarizing current ramp. This was associated with a shift in the start of nonlinearity in the slope resistance to more negative membrane potentials. We proposed that this effect is due to a D1/D5 agonist-induced leftward shift in the activation of INaP. This enables DA to facilitate the firing of PFC neurons in response to depolarizing inputs.




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