Napier T C, Maslowski-Cobuzzi R J
Department of Pharmacology and Experimental Therapeutics, Loyola University Chicago, Stritch School of Medicine, Maywood, Illinois 60153.
Synapse. 1994 Jul;17(3):160-6. doi: 10.1002/syn.890170304.
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.
腹侧苍白球是前脑基部的一个区域，最近研究表明它接受来自中脑的多巴胺能投射。在腹侧苍白球内已确定了D1和D2多巴胺受体家族的结合位点，但激活这些受体的后果尚未得到研究。因此，为了描述腹侧苍白球D1和D2受体亚型的生理药理学特性，在水合氯醛麻醉的大鼠中使用了细胞外单神经元记录和微量离子电泳技术。在接受测试的93个腹侧苍白球神经元中，有一半对多巴胺（DA）的离子电泳敏感，观察到放电频率增加和减少的情况。D1拮抗剂SCH23390或D2拮抗剂舒必利的共离子电泳通常会减弱DA诱导的放电频率变化。与DA一样，接受测试的腹侧苍白球神经元中约有一半对D1激动剂SKF38393敏感。但与DA不同的是，几乎只观察到放电频率抑制，且这种减少的幅度大于DA产生的幅度。SKF38393诱导的抑制作用可被SCH23390拮抗，但不能被舒必利拮抗，这证明了D1激动剂的特异性。大多数接受测试的神经元不受喹吡罗的影响，但当对D2激动剂有反应时，最常观察到放电频率增加。这种增加可被D2拮抗剂舒必利拮抗，但不能被SCH23390拮抗，表明这种反应是由D2受体激活引起的。这些结果支持了结合研究，表明腹侧苍白球中同时存在D1和D2受体，并揭示了分别独立激活其中任何一种受体都足以改变神经元活动。
