(+)-Bicuculline is a light-sensitive competitive antagonist of GABA-A receptor[3]. Bicuculline (25 mM) markedly potentiated Ca2+ transients caused by KCl (25 mM) and by A23187 (4 mM) whereas gabazine (25 mM) had no effect. Bicuculline triggers calcium release when calcium entry is evoked by KCl or A23187 and that this effect is not mediated via GABA(A) receptor blockade[4]. Bicuculline (20-100 micrometers) depressed the GABA-evoked conductance increase in a reversible manner, the double reciprocal transformation of the GABA dose/conductance curves remaining linear. Combinations of bicuculline and picrotoxinin also depressed the GABA response in a manner expected from the combination of two "mixed" non-competitive antagonists. Bicuculline (like picrotoxinin and picrotoxin) behaves as a "mixed" non-competitive rather than a pure non-competitive antagonist of GABA on lobster muscle[5]. Intracerebroventricular administration of 0.3 and 0.5 nmol of bicuculline produces an increase in blood pressure and a slight bradycardia in non-epileptic Wistar rats. The blood pressure response to intracerebroventricular bicuculline is significantly potentiated in epileptic WAG/Rij rats. Additionally, the pressor effect of 0.5 nmol of bicuculline is not attenuated by bilateral electrolytic ablation of the central nucleus of the amygdala in WAG/Rij rats[6].
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