Contribution of presynaptic dopaminergic receptors to the mechanism of the reactivating effects of blockade of the GABA-benzodiazepine-ionophore complex.

Changes in the reactivating efficiency of blockade of components of the GABA-benzodiazepine-ionophore complex were analyzed in conditions of preliminary activation and inhibition of dopamine autoreceptors using (+)ZRRR and haloperidol respectively. A conditioned passive escape reflex was used, along with amnesia produced by detaining mice in the danger sector of a chamber immediately after imposition of a painful stimulus. Doses of bicuculline (1 mg/kg), picrotoxin (1 mg/kg), and flumazenil (10 mg/kg) given before testing restored performance of the conditioned response without altering the neurochemical background. Reductions and increases in dopaminergic activity during the training period prevented restoration of the conditioned passive escape response by blockade of GABAa and benzodiazepine receptors and chloride channels. It is suggested that the neurochemical mechanisms involved in restoring the damaged memory trace are based on the formation of te optimal balance in the activities of the various components of the GABA-benzodiazepine-ionophore complex and the dopaminergic system.