Morgan W W, Pfeil K A
Neuropharmacology. 1984 Jul;23(7A):773-7. doi: 10.1016/0028-3908(84)90110-2.
The intravenous administration of pentobarbital, phenobarbital or barbital produced a dose-related depression of the levels of cyclic guanosine monophosphate (cGMP) in the cerebellum of male Sprague-Dawley rats. This depression of cGMP occurred with doses of pentobarbital and barbital which did not reduce locomotor activity. Further, the time-course of the recovery of locomotor activity following the administration of an anesthetic dose of pentobarbital preceded that for the recovery of the levels cGMP in the cerebellum. In a separate study, pretreatment with picrotoxinin reversed the significant depression of cGMP in the cerebellum produced by the smallest dose of pentobarbital. Collectively, these data suggest that the effects of the barbiturates on cGMP in the cerebellum are not exclusively or predominantly the result of a drug-related depression of locomotor activity and may be, at least partially, mediated via a barbiturate-induced potentiation of a GABA receptor-mediated mechanism.
对雄性斯普拉格-道利大鼠静脉注射戊巴比妥、苯巴比妥或巴比妥，可使小脑内的环磷酸鸟苷（cGMP）水平出现剂量相关的降低。戊巴比妥和巴比妥的这种剂量并未降低运动活性，但却出现了cGMP水平的降低。此外，给予麻醉剂量的戊巴比妥后，运动活性恢复的时间进程先于小脑中cGMP水平恢复的时间进程。在另一项研究中，用印防己毒素预处理可逆转最小剂量戊巴比妥所致的小脑中cGMP的显著降低。总体而言，这些数据表明，巴比妥类药物对小脑中cGMP的影响并非完全或主要是药物相关的运动活性降低的结果，可能至少部分是通过巴比妥类药物诱导的γ-氨基丁酸（GABA）受体介导机制的增强来介导的。
