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首页> 外文期刊>Pharmacology, Biochemistry and Behavior >Distinct inhibition of acute cocaine-stimulated motor activity following microinjection of a group III metabotropic glutamate receptor agonist into the dorsal striatum of rats.
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Distinct inhibition of acute cocaine-stimulated motor activity following microinjection of a group III metabotropic glutamate receptor agonist into the dorsal striatum of rats.

机译：在大鼠背纹状体微注射III型代谢型谷氨酸受体激动剂后，对急性可卡因刺激的运动活动有明显的抑制作用。

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Group III metabotropic glutamate receptors (mGluRs) are negatively coupled to adenylate cyclase through G-proteins. Activation of this group of mGluRs shows an inhibition of dopaminergic transmission in the forebrain. To define the role of striatal group III mGluRs in the regulation of basal and dopamine-stimulated motor behavior, the recently developed agonist and antagonist relatively selective for group III mGluRs were utilized to pharmacologically enhance and reduce group III mGluR glutamatergic tone in the dorsal striatum of chronically cannulated rats. Bilateral injections of a group III agonist, L-2-amino-4-phosphonobutyrate (L-AP4), did not alter basal levels of motor activity at three doses surveyed (1, 10, and 100 nmol). Neither did intracaudate injection of a group III antagonist, alpha-methyl-4-phosphonophenylglycine (MPPG), at 10, 30, and 100 nmol. However, pretreatment with L-AP4 (10 and 100 nmol) dose dependently blocked hyperlocomotion induced by acute injection of cocaine (20 mg/kg, i.p.), amphetamine (2.5 mg/kg, i.p.), or apomorphine (1 mg/kg, s.c.). The behavioral activity induced by cocaine was much more sensitive to L-AP4 than that induced by amphetamine and apomorphine. At 100 nmol, L-AP4 completely blocked cocaine effect whereas amphetamine- and apomorphine-stimulated behaviors were blocked only by 28% and 31%, respectively. The blocking effect of L-AP4 on cocaine action was reversed by pretreatment with MPPG. MPPG itself did not modify behavioral responses to cocaine, amphetamine, or apomorphine. These data indicate that the glutamatergic tone on the group III mGluRs is not active in the regulation of basal and acute dopamine-stimulated motor activity. However, enhanced group III mGluR glutamatergic transmission by an exogenous ligand is capable of suppressing behavioral responses to acute exposure of dopamine stimulants.
机译：III类代谢型谷氨酸受体（mGluRs）通过G蛋白与腺苷酸环化酶负相关。这组mGluRs的激活显示出对前脑中多巴胺能传递的抑制。为了确定纹状体III族mGluRs在调节基础和多巴胺刺激的运动行为中的作用，最近开发的对III族mGluRs具有相对选择性的激动剂和拮抗剂被用于药理增强和减少III型mGluR在大鼠背侧纹状体中的谷氨酸能。慢性插管大鼠。在三个调查剂量（1、10和100 nmol）下，双侧注射III组激动剂L-2-氨基-4-膦酰丁酸酯（L-AP4）不会改变运动活动的基础水平。尾内注射均未在10、30和100 nmol处注射III组拮抗剂α-甲基-4-膦酰基苯基甘氨酸（MPPG）。但是，用L-AP4（10和100 nmol）剂量进行的预处理可依赖性地阻止急性注射可卡因（20 mg / kg，ip），苯丙胺（2.5 mg / kg，ip）或阿扑吗啡（1 mg / kg， sc）。可卡因诱导的行为活性比苯丙胺和阿扑吗啡诱导的对L-AP4更敏感。在100 nmol下，L-AP4完全阻断了可卡因效应，而苯丙胺和阿扑吗啡刺激的行为分别仅被阻断28％和31％。用MPPG预处理可逆转L-AP4对可卡因作用的阻断作用。 MPPG本身并未改变对可卡因，苯丙胺或阿扑吗啡的行为反应。这些数据表明，III类mGluRs上的谷氨酸能基调在调节基础和急性多巴胺刺激的运动活动中没有活性。但是，通过外源配体增强的III组mGluR谷氨酸能传递能够抑制对多巴胺兴奋剂急性暴露的行为反应。

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