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J Neurophysiol 87: 2190-2194, 2002;
0022-3077/02 $5.00
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The Journal of Neurophysiology Vol. 87 No. 4 April 2002, pp. 2190-2194
Copyright ©2002 by the American Physiological Society

RAPID COMMUNICATION

Dopamine Excites Fast-Spiking Interneurons in the Striatum

Enrico Bracci,1,2,3 Diego Centonze,1,2 Giorgio Bernardi,1,2 and Paolo Calabresi1,2

 1Clinica Neurologica, Dipartimento di Neuroscienze, Università "Tor Vergata," Rome 00133;  2Fondazione Santa Lucia, Istituto di Ricovero e Cura a Carattere Scientifico, Rome 00179, Italy; and  3Department of Optometry and Neuroscience, UMIST, Manchester M60 1QD, United Kingdom

Bracci, Enrico, Diego Centonze, Giorgio Bernardi, and Paolo Calabresi. Dopamine Excites Fast-Spiking Interneurons in the Striatum. J. Neurophysiol. 87: 2190-2194, 2002. The striatum is the main recipient of dopaminergic innervation. Striatal projection neurons are controlled by cholinergic and GABAergic interneurons. The effects of dopamine on projection neurons and cholinergic interneurons have been described. Its action on GABAergic interneurons, however, is still unknown. We studied the effects of dopamine on fast-spiking (FS) GABAergic interneurons in vitro, with intracellular recordings. Bath application of dopamine elicited a depolarization accompanied by an increase in membrane input resistance (an effect that persisted in the presence of tetrodotoxin) and action-potential discharge. These effects were mimicked by the D1-like dopamine receptor agonist SKF38393 but not by the D2-like agonist quinpirole. Evoked corticostriatal glutamatergic synaptic currents were not affected by dopamine. Conversely, GABAergic currents evoked by intrastriatal stimulation were reversibly depressed by dopamine and D2-like, but not D1-like, agonists. Cocaine elicited effects similar to those of dopamine on membrane potential and synaptic currents. These results show that endogenous dopamine exerts a dual excitatory action on FS interneurons, by directly depolarizing them (through D1-like receptors) and by reducing their synaptic inhibition (through presynaptic D2-like receptors).




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