Electrophysiological verification of the presence of D1 and D2 dopamine receptors within the ventral pallidum.
Electrophysiological verification of the presence of D1 and D2 dopamine receptors within the ventral pallidum.
复制标题
腹侧苍白球内 D1 和 D2 多巴胺受体存在的电生理学验证。
DOI：
10.1002/syn.890170304
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发表时间：
1994
期刊：
影响因子：
--
通讯作者：
Maslowski-Cobuzzi,RJ
中科院分区：
文献类型：
--
作者：
Napier,TC;Maslowski-Cobuzzi,RJ
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. © 1994 Wiley‐Liss. Inc.
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DOI：
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期刊：
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