Abramets I I, Komissarov I V
Biull Eksp Biol Med. 1985 Jun;99(6):698-700.
It has been established in experiments on the isolated spinal cord of 7-14-day-old rats that the GABAB-mimetic phenibut (10(-5)--10(-4) M) elicits a slow-developing depolarization of motoneurons, suppression of spontaneous activity and polysynaptic reflex discharges of motoneurons, recorded from the ventral roots. Administered under the same conditions GABA produces de- and hyperpolarization of motoneurons. The depolarization of motoneurons elicited by phenibut and GABA is not reversed by picrotoxin in contradistinction to the GABA-induced hyperpolarization of motoneurons, being associated with a direct action of the GABA-mimetics on postsynaptic GABAB receptors of motoneurons. Diazepam (10(-9)--10(-6) M) potentiates the effects of phenibut supposedly via benzodiazepine receptors bound with GABAA receptors (an independent interaction).
在对7至14日龄大鼠的离体脊髓进行的实验中已证实,GABAB模拟物苯乙哌啶酮(10(-5)--10(-4)M)可引起运动神经元缓慢发展的去极化,抑制从腹根记录到的运动神经元的自发活动和多突触反射放电。在相同条件下给予的GABA会使运动神经元产生去极化和超极化。与GABA诱导的运动神经元超极化不同,苯乙哌啶酮和GABA引起的运动神经元去极化不会被苦味毒逆转,这与GABA模拟物对运动神经元突触后GABAB受体的直接作用有关。地西泮(10(-9)--10(-6)M)可能通过与GABAA受体结合的苯二氮䓬受体(一种独立的相互作用)增强苯乙哌啶酮的作用。