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首页> 外文期刊>Pharmacology, Biochemistry and Behavior >The role of serotonin(2) receptors in mediating cocaine-induced convulsions.
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The role of serotonin(2) receptors in mediating cocaine-induced convulsions.

机译：血清素（2）受体在介导可卡因诱发的惊厥中的作用。

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Previous research in our laboratory suggests that serotonin (5-HT) neurotransmission mediates the expression of cocaine-induced convulsions. The role of 5-HT in mediating this toxic effect of cocaine appears to be due to activation of 5-HT(2) receptors, because cocaine-induced convulsions are blocked by the 5-HT(2) antagonists cinanserin, ketanserin, and pirenperone. The present study utilized a number of compounds that display a high affinity for 5-HT(2) receptors to further examine the role of these sites in mediating this toxic effect of cocaine. Cocaine-induced convulsions were observed following pretreatment with various doses of the following 5-HT(2) antagonists: mianserin, metergoline, MDL 11939, and methiothepin. In addition, 1-(2-methoxyphenyl)-4-[4-(2-phthalimido)butyl]piperazine (NAN 190) was tested to examine the influence of 5-HT(1) sites and the agonist compound 1-(3-triflurormethylphenyl)piperazine (TFMPP) was examined to further explore the role of 5-HT(1) and 5-HT(2) sites. Each 5-HT(2) antagonist attenuated cocaine-induced convulsions. Conversely, NAN 190 did not alter this toxic effect of cocaine. In addition, TFMPP significantly potentiated cocaine-induced convulsions. The results from this study support the hypothesis that 5-HT neurotransmission, acting primarily at 5-HT(2) receptors, plays an important role in mediating cocaine-induced convulsions.
机译：我们实验室先前的研究表明，血清素（5-HT）神经传递介导可卡因诱发的惊厥的表达。 5-HT介导可卡因毒性作用的作用似乎是由于5-HT（2）受体的激活所致，因为可卡因诱发的惊厥被5-HT（2）拮抗剂cinanserin，ketanserin和pirenperone阻断。本研究利用了许多对5-HT（2）受体具有高亲和力的化合物，以进一步检查这些位点在介导可卡因毒性作用中的作用。在用各种剂量的以下5-HT（2）拮抗剂进行预处理后，观察到可卡因引起的惊厥：棉胺素，美特古林，MDL 11939和美托西平。另外，还测试了1-（2-甲氧基苯基）-4- [4-（2-邻苯二甲酰亚胺基）丁基]哌嗪（NAN 190），以研究5-HT（1）位点和激动剂化合物1-（3 -三氟甲基苯基）哌嗪（TFMPP）被检查以进一步探索5-HT（1）和5-HT（2）网站的作用。每个5-HT（2）拮抗剂减弱可卡因诱发的抽搐。相反，NAN 190并没有改变可卡因的这种毒性作用。此外，TFMPP显着增强了可卡因诱发的惊厥。这项研究的结果支持以下假设：5-HT神经传递主要作用于5-HT（2）受体，在介导可卡因诱发的惊厥中起重要作用。

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