Glutamic acid and histamine-sensitive neurons in the ventral hippocampus and the basolateral amygdala of the rat: functional interaction on memory and learning processes

Abstract

The possibility of a functional interaction between the amygdala and the ventral hippocampus during learning of a conditioned avoidance response when both brain structures are chemically stimulated with glutamic acid and/or histamine receptor antagonists (pyrilamine, H1-histamine antagonist and ranitidine, H2-histamine receptor antagonist) was studied in rats. Adult male rats were stereotaxically implanted with guide cannulae into the basolateral amygdala (A) and the ventral hippocampus (H). Seventy-two hours after the implant, rats were microinjected with 1 microl of saline solution, 10 nmol glutamic acid or 45 nmol of histamine receptor antagonists in several brain structures combinations. These combinations were: HsalAsal; HmsgAmsg; HmsgAsal; HsalAmsg; HpyrAmsg; HmsgApyr; HranAmsg and HmsgAran. Five minutes after the injection, rats were subjected to a learning task which consisted to avoid an electric shock applied to the animal's feet when an ultrasonic tone of 40 kHz is on for 30 s. Results showed that the simultaneous application of glutamic acid into hippocampus and amygdala interfered with the latency to escape and memory consolidation process. Stimulation with glutamic acid alone into the hippocampus or into the amygdala (HsalAmsg and HmsgAsal groups) interfered slightly with latency but impaired the consolidation process. Blocking the H1-histamine receptors of the amygdala affected slightly latency and efficiency of learning, meanwhile the blocking of H2-histamine receptors interfered with both parameters. Blocking H1- and H2-histamine receptors of the hippocampus significantly impaired latency and efficiency of learning of rats stimulated with glutamic acid into the amygdala. In conclusion, the experimental evidence suggests that hippocampal glutamic acid-neurons functionally interact with histamine-neurons in the basolateral amygdala to modulate memory and learning process.