Metabolism and Receptor Binding of Serotonin in Brain Structures During Performance of a Conditioned Passive Avoidance Response

Abstract

The levels of serotonin and its metabolite 5-hydroxyindoleacetic acid, monoamine oxidase activity, and the specific binding of the radioligand [3H]serotonin were measured in the prefrontal cortex, striatum, amygdaloid complex, hippocampus, and periacqueductal gray matter of the midbrain in rats at different time points after training to a conditioned passive avoidance reaction. Changes in serotoninergic activity were found to be characteristic only for the process of reproducing the conditioned reaction. The metabolism and serotonin receptor binding in these brain structures did not change immediately after the training period or one day after this, or in conditions of failure to reproduce the reaction because of amnesia, or in untrained animals. The involvement of the brain serotoninergic system in the process of performing the conditioned reaction was found to demonstrate a spatial-structural selectivity: the metabolism and receptor binding of serotonin changed in the amygdaloid complex, periacqueductal gray matter, and the striatum, while no changes were seen in the hippocampus or prefrontal cortex. All three brain structures showed decreases in [3H]serotonin receptor binding of. Serotonin levels did not change, though the amygdaloid complex and periacqueductal gray matter showed increases in oxidative deamination of serotonin and increases in the active transport of the metabolite, while the striatum showed decreases in serotonin catabolism. The differences in the catabolism of this neurotransmitter suggest that the decrease in serotonin receptor binding in these brain structures depends on different synaptic processes--presynaptic in the striatum and postsynaptic in the amygdaloid complex and periacqueductal gray matter. It is concluded that the decrease in the functional activity of serotoninergic transmission in the amygdaloid complex and periacqueductal gray matter is one of the mechanisms involved in activation of the emotiogenic system triggering the process of reproduction of the memory trace.