Electrophysiological verification of the presence of D1 and D2 dopamine receptors within the ventral pallidum.
The ventral pallidum is a basal forebrain region recently shown to receive dopaminergic projections from the midbrain. Binding sites for the D1 and D2 dopamine receptor families have been identified within the ventral pallidum, yet the consequences of activating these receptors have not been studied. Thus, to characterize the physiological pharmacology of D1 and D2 receptor subtypes for the ventral pallidum, extracellular single-neuron recording and microiontophoretic techniques were used in chloral hydrate-anesthetized rats. Half of the 93 ventral pallidal neurons tested were sensitive to iontophoresis of dopamine (DA), and both rate increases and decreases were observed. Co-iontophoresis of either the D1 antagonist SCH23390, or the D2 antagonist sulpiride, generally attenuated the DA-induced rate changes. Like DA, about half of the ventral pallidal neurons tested were sensitive to the D1 agonist, SKF38393. Yet in contrast to DA, rate suppression was observed almost exclusively, and the magnitude of this decrease was greater than that produced by DA. SKF38393-induced suppressions were antagonized by SCH23390, but not by sulpiride, demonstrating the specificity of the D1 agonist. Most of the neurons tested were not affected by quinpirole, but when responsive to the D2 agonist, rate increases were observed most often. The increases were antagonized by the D2 antagonist sulpiride, but not SCH23390, demonstrating that this response resulted from an activation of D2 receptors. These results support binding studies demonstrating that both D1 and D2 receptors are present in the ventral pallidum, and reveal that the independent activation of each of these is sufficient to alter neuronal activity.
Department of Pharmacology and Experimental Therapeutics, Loyola University Chicago, Stritch School of Medicine, Maywood, Illinois 60153.
T C
TC
Napier
R J
RJ
Maslowski-Cobuzzi
D015647:2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine / Q000494:pharmacology; D000818:Animals; D004298:Dopamine / Q000494:pharmacology; D018491:Dopamine Agonists / Q000494:pharmacology; D065127:Dopamine D2 Receptor Antagonists; D004594:Electrophysiology; D004873:Ergolines / Q000494:pharmacology; D005917:Globus Pallidus / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D007478:Iontophoresis; D008297:Male; D009474:Neurons / Q000187:drug effects; D019257:Quinpirole; D051381:Rats; D017207:Rats, Sprague-Dawley; D017447:Receptors, Dopamine D1 / Q000819:agonists / Q000037:antagonists & inhibitors / Q000502:physiology*; D017448:Receptors, Dopamine D2 / Q000819:agonists / Q000502:physiology*
D018491:Dopamine Agonists; D065127:Dopamine D2 Receptor Antagonists; D004873:Ergolines; D017447:Receptors, Dopamine D1; D017448:Receptors, Dopamine D2; D019257:Quinpirole; D015647:2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine; D004298:Dopamine