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首页> 外文期刊>Pharmacology, Biochemistry and Behavior >Differential modulatory actions of GABAA agonists on susceptibility to GABAA antagonists-induced seizures in morphine dependent rats: Possible mechanisms in seizure propensity.
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Differential modulatory actions of GABAA agonists on susceptibility to GABAA antagonists-induced seizures in morphine dependent rats: Possible mechanisms in seizure propensity.

机译：GABAA激动剂对吗啡依赖性大鼠对GABAA拮抗剂诱发的癫痫发作敏感性的差异性调节作用：癫痫发作倾向的可能机制。

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In order to clarify the mechanisms involved in the susceptibility to GABA(A) antagonists-induced seizures in morphine dependent rats, we investigated how GABA(A) agonists modulate this vulnerability. Seizures were induced to animals by infusion of GABA(A) antagonists: pentylenetetrazole (PTZ), picrotoxin (PIC) and bicuculline (BIC). GABA(A) agonists, muscimol (MUS) and 4,5,6,7-tetrahydroisoxazolo [5,4-c]pyridin-3-ol (THIP), were administered intravenous (i.v.) before antagonists. Morphine-dependence significantly decreased the PTZ threshold dose (19.16+/-1.89 versus 25.74+/-1.25mg/kg) while, it had no effect on PIC induced seizures. BIC doses for both threshold and tonic-clonic seizures induction were significantly lower in morphine dependent rats (0.10+/-0.01 and 0.12+/-0.02 versus 0.25+/-0.02 and 0.39+/-0.07mg/kg respectively). In morphine-dependence, although pre-treatment with MUS significantly increased the required dose of PTZ for seizures threshold, THIP significantly decreased the required dose of PTZ for tonic-clonic convulsion. Moreover, MUS pretreatment completely recovered the effect of morphine dependency on BIC seizure activity. The results suggest that the capability of GABA(A) agonists on modulation of propensity to seizures induced by different antagonists in morphine-dependence is dissimilar. Therefore, it seems that long-term morphine alters some properties of GABA system so that the responsive rate of GABA(A) receptors not only to its antagonists, but also to its agonists will change differently.
机译：为了阐明在吗啡依赖性大鼠中对GABA（A）拮抗剂诱导的癫痫发作易感性的机制，我们研究了GABA（A）激动剂如何调节此脆弱性。通过输注GABA（A）拮抗剂：戊四氮（PTZ），微毒素（PIC）和小瓜碱（BIC）诱发癫痫发作。在拮抗剂之前，静脉内（i.v.）施用GABA（A）激动剂，麝香酚（MUS）和4,5,6,7-四氢异恶唑[5,4-c]吡啶-3-醇（THIP）。吗啡依赖性显着降低PTZ阈值剂量（19.16 +/- 1.89对25.74 +/- 1.25mg / kg），而对PIC诱发的癫痫发作没有影响。在吗啡依赖性大鼠中，阈值诱导和强直-阵挛性癫痫发作的BIC剂量均显着降低（分别为0.10 +/- 0.01和0.12 +/- 0.02，而0.25 +/- 0.02和0.39 +/- 0.07mg / kg）。在吗啡依赖性方面，尽管用MUS预处理显着增加了癫痫发作阈值所需的PTZ剂量，但是THIP显着降低了强直-阵挛性惊厥所需的PTZ剂量。此外，MUS预处理完全恢复了吗啡依赖性对BIC癫痫发作活动的影响。结果表明，GABA（A）激动剂对吗啡依赖性不同拮抗剂诱导的癫痫发作倾向的调节能力不同。因此，长期的吗啡似乎改变了GABA系统的某些特性，因此GABA（A）受体不仅对其拮抗剂而且对激动剂的响应率也会发生不同的变化。

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