The role of GABAA and GABAB receptors in the development of amnesia.

It has been demonstrated that a gradual spontaneous recovery of a previously unreproducible memory trace and the prevention of the antiamnesic effect of the blockade of the GABAA receptor, but not of the blockade of the benzodiazepine receptor or the chloride channel, take place with the development of amnesia against the background of the activation of the GABAB receptor by baclofen. The "neurochemical set" created by the activation of the GABAA receptor by muscimol in a dose of 1 mg/kg prevents the antiamnesic effect of the blockade of any component of the benzodiazepine-GABA-ionophore complex, while at a dose of muscimol of 0.5 mg/kg, the retrieval of the amnestic trace takes place only by blockade of the benzodiazepine receptor. Thus, the development of amnesia is determined by the functional state of inhibitory GABAergic systems of the brain, which governs the subsequent correction of the amnestic memory trace.