Pre- and postsynaptic mechanisms of the involvement of amygdaloid complex serotonin in the reproduction of a conditioned passive avoidance response in rats.

Serotonin metabolism and [3H]-serotonin radioligand receptor binding were studied in the amygdaloid complex of the rat brain at different stages of a conditioned passive avoidance response. Serotoninergic changes were specific for the process of reproduction of the conditioned response. The involvement of serotonin in the amygaloid complex during reproduction of memory traces consisted of a reduction in its postsynaptic receptor binding.

Molecular basis of the activity of the dopamine synapse in the mechanisms of learning and amnesia.

The neurochemical correlates of dopamine synapse activity were studied during the retrieval of memory traces and in the absence of retrieval ("psychogenic" amnesia). The physiochemical parameters of D2 receptor function, the synaptic membrane, and the catechol content were assessed in various regions of the brain (striatum, neostriatum, hypothalamus, amygdala, frontal cortex, hippocampus, nucleus accumbens, and nuclei A9 and A10) in intact, trained, and amnesiac rats. It was demonstrated that disturbances in memory trace retrieval were associated with decreased activation of synaptic dopamine receptors and alterations in the dopamine transformation pathway in the rat brain.

Interaction of serotonin- and dopaminergic systems of the brain in mechanisms of latent inhibition in rats.

The activity of serotoninergic neurons of the medial raphé nucleus was turned off by local injection of the neurotoxin, 5,7-dihydroxytryptamine. Seven days later, a conditioned passive avoidance reaction was developed following 20 preexposures to the conditional stimulus (the presentation of the experimental chamber). As compared with the sham-operated control, in which 20 preexposures to the stimulus elicited latent inhibition, i.

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.

Influence of changes in the effectiveness of blockade of the benzodiazepine-GABA ionophore complex on the reproduction of the amnestic memory trace in mice after preliminary administration of diazepam.

A comparative analysis was carried out in experiments on mice, using the methodology of the conditioned passive avoidance reaction, of the effectiveness of the blockade of the BD-GABA ionophore complex and its individual components in the recovery of a memory trace following "psychogenic" amnesia developing against the background of preliminary activation of BD-receptors by diazepam. It was shown that an improvement in the reproduction of the conditioned reaction was observed on the second day under conditions of "neurochemical tuning" only with the blockade of the GABAA receptor by bicuculline. Flumazepil and picrotoxin did not elicit an improvement in the reproduction of the reaction.