Influence of thyrotropin releasing hormone and histidyl-proline diketopiperazine on spontaneous locomotor activity and analgesia induced by delta 9-tetrahydrocannabinol in the mouse.
Influence of thyrotropin releasing hormone and histidyl-proline diketopiperazine on spontaneous locomotor activity and analgesia induced by delta 9-tetrahydrocannabinol in the mouse.
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促甲状腺激素释放激素和组氨酰脯氨酸二酮哌嗪对 δ9-四氢大麻酚诱导的小鼠自发运动活性和镇痛的影响。
DOI：
10.1016/0014-2999(80)90315-5
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发表时间：
1980
影响因子：
5
通讯作者：
Matwyshyn,GA
中科院分区：
文献类型：
--
作者：
Bhargava,HN;Matwyshyn,GA
本文观察了促甲状腺激素释放激素（TRH）及其代谢产物组氨酰脯氨酸二酮哌嗪（HPD）对Δ9-四氢大麻酚（THC）镇静镇痛作用的影响。脑内注射HPD（10 μg）可单独降低运动活动，而TRH（10 μg）则无此作用。腹腔注射THC（10和20 mg/kg）可降低运动活动，这种作用可被TRH或HPD预先治疗所拮抗。四氢大麻酚的管理产生镇痛证明了延迟甩尾反应时间的热刺激。TRH或HPD预处理也可拮抗THC的镇痛作用。THC诱导的镇痛作用不受s.c.用纳洛酮（一种阿片拮抗剂）预处理。TRH或HPD预处理对THC及其代谢物在脑和血浆中的总放射性分布没有影响。这些研究表明，TRH和HPD可拮抗THC的镇静镇痛作用，HPD可能是TRH的活性代谢产物。观察到这些作用，但未改变药物在脑和血浆中的分布和代谢，因此其作用可能涉及其对中枢神经系统的直接作用。最后，THC诱导的镇痛似乎不涉及阿片受体，它们参与TRH或HPD拮抗THC诱导的镇痛的机制是不可能的。
The influence of thyrotropin releasing hormone (TRH) and its postulated metabolite histidyl-proline diketopiperazine (HPD) on sedation and analgesia produced byΔ9-tetrahydrocannabinol (THC) was investigated in mice. Intracerebral administration of HPD (10 μg) by itself decreased motor activity, whereas, TRH (10 μg) was without any effect. THC (10 and 20 mg/kg) given i.p. decreased the motor activity and this effect was antagonised by prior treatment with TRH or HPD. Administration of THC produced analgesia as evidenced by delay in the tail-flick reaction time to a thermal stimulus. Pretreatment with TRH or HPD also antagonized the THC-induced analgesia. THC-induced analgesia was not modified by s.c. pretreatment with naloxone, an opiate antagonist. TRH or HPD pretreatment had no effect on the distribution of total radioactivity representing THC and its metabolites in brain and plasma. These studies indicate that TRH and HPD can antagonize THC-induced sedation and analgesia and that HPD may be an active metabolite of TRH. These effects were observed without altering the distribution of the drug and metabolic in brain and plasma and therefore their effect may involve their direct actions on the central nervous system. Finally THC induced analgesia does not seem to involve opiate receptors and their involvement in the mechanism by which TRH or HPD antagonize THC-induced analgesia is unlikely.
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