Dopamine and endogenous opioid regulation of picrotoxin-induced locomotion in the ventral pallidum after dopamine depletion in the nucleus accumbens.
Dopamine and endogenous opioid regulation of picrotoxin-induced locomotion in the ventral pallidum after dopamine depletion in the nucleus accumbens.
复制标题
伏隔核多巴胺耗竭后，多巴胺和内源性阿片类药物对印防己毒素诱导的腹侧苍白球运动的调节。
DOI：
10.1007/bf02245299
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发表时间：
1992
影响因子：
3.4
通讯作者：
Kalivas,PW
中科院分区：
文献类型：
--
作者：
Churchill,L;Austin,MC;Kalivas,PW
将微微毒素或μ-阿片激动剂Tyr-D-Ala-Gly-NmePhe-Gly-OH （DAMGO）微注射到腹侧白质（VP）中，可引起运动活性增加，并被多巴胺受体阻断拮抗。为了研究伏隔核多巴胺能神经支配对vp诱导运动的调控以及阿片受体在这一调控中的作用，我们采用6-羟基多巴胺（6-OHDA）损伤双侧伏隔核多巴胺神经。与假损伤大鼠相比，损伤导致伏隔核组织多巴胺水平下降89-97%。NA中的多巴胺缺失不能显著拮抗注射到VP中的微毒素或DAMGO。然而，多巴胺受体拮抗剂氟哌啶醇（0.1 mg/kg， IP）在假性和6-羟多巴胺损伤的大鼠中，阻断了微曲毒素引起的水平光细胞计数的增加。阿片受体拮抗剂纳洛酮（1.0 mg/kg， SC）也能阻断6-羟多巴胺损伤大鼠的运动，但不能阻断假损伤大鼠的运动。在更高剂量（3.0 mg/kg， SC）下，纳洛酮阻断了假性和6-羟色胺损伤大鼠的picrotoxin诱导的运动。这些结果表明，虽然NA中的多巴胺消耗不会影响多巴胺传递对VP引起的运动的允许作用，但它会导致对脑啡能传递的敏感性增加。
Microinjection of picrotoxin or the μ-opioid agonist, Tyr-D-Ala-Gly-NmePhe-Gly-OH (DAMGO), into the ventral pallidum (VP) produces an increase in locomotor activity that is antagonized by dopamine receptor blockade. To investigate the regulation of VP-induced locomotion by the dopaminergic innervation of the nucleus accumbens (NA) and the role of opioid receptors in this regulation, dopamine innervation of the NA was bilaterally lesioned with 6-hydroxydopamine (6-OHDA). The lesions resulted in an 89–97% depletion of tissue dopamine levels in the nucleus accumbens compared with sham-lesioned rats. Dopamine depletion in the NA failed to significantly antagonize picrotoxin or DAMGO injected into the VP. However, the dopamine receptor antagonist, haloperidol (0.1 mg/kg, IP), blocked the picrotoxin-initiated increase in horizontal photocell counts in both sham- and 6-OHDA-lesioned rats. The opioid receptor antagonist, naloxone (1.0 mg/kg, SC), also blocked the picrotoxin-induced locomotion in 6-OHDA-lesioned rats but did not block locomotion in the sham-lesioned rats. At a higher dose (3.0 mg/kg, SC), naloxone blocked picrotoxin-induced locomotion in both sham- and 6-OHDA-lesioned rats. These results indicate that although dopamine depletion in the NA does not affect the permissive role of dopamine transmission on locomotion elicited from the VP, it results in an increased sensitivity to enkephalinergic transmission.