Elsevier

Neuroscience Letters

Volume 224, Issue 1, 7 March 1997, Pages 61-65
Neuroscience Letters

Dopamine enhances glutamate-induced excitation of rat striatal neurons by cooperative activation of D1 and D2 class receptors

https://doi.org/10.1016/S0304-3940(97)13443-7Get rights and content

Abstract

Although dopamine (DA) usually inhibits firing of rat striatal neurons in vivo, iontophoresis of DA with low ejection currents can also potentiate glutamate-evoked activity. We used extracellular single cell recording to examine the DA receptor subtypes involved in such potentiation. At low iontophoretic currents (1–8 nA), both the DA D1 class receptor agonist SKF 38393 and the DA D2 class receptor agonist quinpirole mimicked the ability of DA to facilitate glutamate-induced activity. Acute depletion of DA abolished the excitatory modulation produced by either D1 or D2 agonists but not by DA. Co-administration of SKF 38393 and quinpirole restored the facilitation of glutamate effects in DA-depleted rats. Stimulation of both D1 and D2 class receptors appears to be required for DA to enhance glutamate-induced firing of striatal neurons.

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Acknowledgements

This research was supported by USPHS Grants DA-04093 and MH-40832 to F.J.W. who is also a recipient of a National Institute on Drug Abuse Research Scientist Development Award (DA 00207).

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