Further evidence for GABA-ergic mechanisms in the action of benzodiazepines.
Drugs of the benzodiazepine series (clonazepam, lorazepam, diazepam and medazepam) increase the inhibitory processes in the cerebral cortex as it has been shown by means of the recovery cycles of the intracortical response. There is a correlation between the effect on the recovery cycles and their protective action against convulsions induced by GABA deficit. Diazepam enhances the inhibitory effect of GABA applied iontophoretically to rabbit sensorymotor cortex neurons. The drug GABA-ergic effect seems to be specific since it fails to modify the effects of other putative neurotransmitters (glutamate, glycine, acetylcholine). The alteration of rat conflict situation behaviour under diazepam has been eliminated due to the blockade of GABA-receptors by gicuculline and the decrease of the GABA level by thiosemicarbazide. It is inferred that the main effects of benzodiazepines are mediated by GABA and suggested that these agents increase the sensitivity of postsynaptic GABA-ergic receptors.
Further evidence for GABA-ergic mechanisms in the action of benzodiazepines. Drugs of the benzodiazepine series (clonazepam, lorazepam, diazepam and medazepam) increase the inhibitory processes in the cerebral cortex as it has been shown by means of the recovery cycles of the intracortical response. There is a correlation between the effect on the recovery cycles and their protective action against convulsions induced by GABA deficit. Diazepam enhances the inhibitory effect of GABA applied iontophoretically to rabbit sensorymotor cortex neurons. The drug GABA-ergic effect seems to be specific since it fails to modify the effects of other putative neurotransmitters (glutamate, glycine, acetylcholine). The alteration of rat conflict situation behaviour under diazepam has been eliminated due to the blockade of GABA-receptors by gicuculline and the decrease of the GABA level by thiosemicarbazide. It is inferred that the main effects of benzodiazepines are mediated by GABA and suggested that these agents increase the sensitivity of postsynaptic GABA-ergic receptors.