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γ-氨基丁酸氯离子通道成分在雄蟹攻击行为中的作用

Role of the GABA chloride ion channel component on aggressive behavior in the male crab.

作者信息

Canonaco M, Bergamo P, Tavolaro R, Miralto A

机构信息

Dipartimento di Ecologia, Università della Calabria, Roges di Rende (CS), Italy.

出版信息

Physiol Behav. 1991 Mar;49(3):411-5. doi: 10.1016/0031-9384(91)90257-o.

DOI:10.1016/0031-9384(91)90257-o
PMID:1648238
Abstract

Picrotoxin blocking effects on GABA-induced inhibition of lateral merus display in the male crab Carcinus mediterraneus suggest that the chloride ion channel component of the GABA molecule is involved in the control of this defensive behavior. The low GABA doses (3 and 5 micrograms/g body weight) inhibited lateral merus display as early as 10 min after drug treatment while the administration of higher GABA concentrations (greater than 5 micrograms/g) prolonged the duration of the behavioral effects. The administration of 1 microgram/g picrotoxin to the animals treated with the effective GABA doses (5, 10 and 20 micrograms/g) restored lateral merus display. The antagonizing activity of picrotoxin on the inhibitory GABA effects, in a temporal manner, demonstrates that GABAergic sites other than peripheral ones are probably participating with the regulation of this agonistic posture. Quantitative autoradiography results revealed interesting receptor levels changes of the specific chloride ion channel antagonist [35S] t-butylbicyclophosphorothionate in the different brain areas of the male crab displaying lateral merus with respect to normal nonreactive animals. Elevated receptor binding levels were encountered in the middle and posterior brain area whereas low levels were obtained at the anterior level. Both the behavioral and autoradiographic results suggest that the defensive type of aggression behavior in crustacean may not only be mediated by a peripherally controlled GABA-gated chloride ion flux but also by a central GABAergic mechanism.

摘要

印防己毒素对地中海雄蟹侧螯足展示中γ-氨基丁酸(GABA)诱导的抑制作用表明,GABA分子的氯离子通道成分参与了这种防御行为的控制。低剂量的GABA(3和5微克/克体重)在药物处理后10分钟就抑制了侧螯足展示,而给予更高浓度的GABA(大于5微克/克)则延长了行为效应的持续时间。对用有效剂量的GABA(5、10和20微克/克)处理的动物给予1微克/克的印防己毒素,恢复了侧螯足展示。印防己毒素对GABA抑制作用的拮抗活性,从时间上看,表明除外周部位外的GABA能位点可能参与了这种争斗姿势的调节。定量放射自显影结果显示,与正常无反应的动物相比,展示侧螯足的雄蟹不同脑区中特异性氯离子通道拮抗剂[35S]叔丁基双环磷硫酯的受体水平发生了有趣的变化。在中脑和后脑区域发现受体结合水平升高,而在前脑区域则较低。行为学和放射自显影结果均表明,甲壳类动物的防御性攻击行为可能不仅由外周控制的GABA门控氯离子通量介导,还由中枢GABA能机制介导。

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