Zharkovsky A, Cebers G
Department of Pharmacology, Tartu University, Estonia.
Alcohol Alcohol Suppl. 1993;2:483-7.
The termination of chronic ethanol administration in rats resulted in the development of withdrawal signs at 10 and 24 hours of withdrawal. The behavioural signs of withdrawal were accompanied by an increased potassium-evoked 45Ca2+ uptake by cortical synaptoneurosomes. The dihydropyridine calcium channel antagonist nifedipine given acutely, suppressed the withdrawal signs and abolished the increased 45Ca2+ uptake. The benzodiazepine receptor inverse agonist Ro 15-4513 (4 mg/kg) given at 1.5 hours after termination of chronic ethanol induced behavioural signs of withdrawal and increased potassium-evoked 45Ca2+ uptake in these animals. Ro 15-45-13 given at 24 hours of withdrawal did not further enhance withdrawal signs or 45Ca2+ uptake. These data suggest that an increased calcium uptake during ethanol withdrawal might be attributed to the activation of dihydropyridine-sensitive calcium channels and might be involved in the development of withdrawal signs after chronic ethanol administration.
大鼠长期给予乙醇后停药，在停药10小时和24小时出现戒断症状。戒断的行为症状伴有皮质突触神经小体对钾诱发的45Ca2+摄取增加。急性给予二氢吡啶类钙通道拮抗剂硝苯地平可抑制戒断症状，并消除增加的45Ca2+摄取。在长期乙醇给药结束后1.5小时给予苯二氮䓬受体反向激动剂Ro 15 - 4513（4mg/kg）可诱发这些动物出现戒断行为症状，并增加钾诱发的45Ca2+摄取。在停药24小时给予Ro 15 - 45 - 13不会进一步加重戒断症状或增加45Ca2+摄取。这些数据表明，乙醇戒断期间钙摄取增加可能归因于二氢吡啶敏感性钙通道的激活，并且可能参与长期乙醇给药后戒断症状的发生。
