Limbic pallidal adaptations following long-term cessation of dopaminergic transmission: lack of upregulation of dopamine receptor function.
Limbic pallidal adaptations following long-term cessation of dopaminergic transmission: lack of upregulation of dopamine receptor function.
复制标题
多巴胺能传递长期停止后边缘苍白球适应：缺乏多巴胺受体功能的上调。
DOI：
10.1016/j.expneurol.2003.11.004
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发表时间：
2004
影响因子：
5.3
通讯作者：
Napier,TCeleste
中科院分区：
文献类型：
--
作者：
Heidenreich,ByronA;Mitrovic,Igor;Battaglia,George;Napier,TCeleste
Neurons in the ventral pallidum (VP) exhibit robust responding to activation of dopamine (DA) receptors of the D1class. To determine if the VP adapts to chronic cessation of DA transmission, the present studies examined D1receptor-mediated responses in the VP recorded extracellularly in chloral-hydrate anesthetized rats following destruction of DA neurons with 6-hydroxydopamine (6-OHDA) or long-term treatment with the D1antagonist SCH23390. Indices of basal spiking (i.e., spontaneous firing rate and pattern) recorded 10–21 days after unilateral 6-OHDA treatment did not differ from controls. Moreover, DA depletion did not alter the proportion of VP neurons whose rate was enhanced with iv injections of the D1agonist SKF38393, and the functional efficacy (Emax) and potency (ED50) were similar to controls. There also was no change in the direction of responses, the Emaxor the ED50measure of sensitivity (ECur50) to iontophoretic application of DA or SKF38393 in VP neurons. Forty-eight hours after 21 once-daily treatments with SCH23390, the number of [3H]SCH23390-labeled D1receptors was increased in the striatum, but unchanged in the VP, globus pallidus, or septum. Accordingly, there was no functional upregulation of VP responses to iv SKF38393. Indeed, the proportion of SKF38393-sensitive neurons was decreased after chronic SCH23390. Distinguishing the VP from other forebrain regions, these findings indicate that basal spiking is not altered in the VP following chronic DA depletion, and that no upregulation of VP DA receptor function occurs following either dopaminergic lesions or chronic antagonism of D1receptors.
