Dexamethasone reverses the memory impairment induced by antagonism of hippocampal gastrin-releasing peptide receptors.

Storage of emotionally influenced memory is regulated by activation of glucocorticoid receptors (GRs) as well as of gastrin-releasing peptide receptors (GRPRs) in the dorsal hippocampus. In the present study, male Wistar rats were given a bilateral infusion of saline or the GRPR antagonist (D-Tpi6, Leu13 psi[CH2NH]-Leu14) bombesin (6-14) (RC-3095) (1.0 microg/side) into the dorsal hippocampus 10 min before training on an inhibitory avoidance task, followed by an immediate post-training i.p. injection of vehicle or the GR agonist dexamethasone (0.3 mg/kg). A retention test trial, carried out 24 h after training, indicated that intrahippocampal infusion of RC-3095 impaired inhibitory avoidance retention. Post-training administration of dexamethasone induced an enhancement of retention regardless of whether the animals had received saline or RC-3095 into the hippocampus before training. The findings indicate that hippocampal GRPR blockade does not prevent memory enhancement induced by dexamethasone. Together with previous results, these findings suggest that endogenous activation of GRPRs in the hippocampus modulates the consolidation of emotional memory, but is not a critical receptor system mediating memory formation.

Bombesin/gastrin-releasing peptide receptors in the basolateral amygdala regulate memory consolidation.

Several receptor and intracellular signalling systems in the basolateral amygdala (BLA) regulate memory formation. In the present study, we show that bombesin/gastrin-releasing peptide (GRP) receptors in the BLA are involved in the consolidation of affectively motivated memory. Adult male rats were trained in a single-trial step-down inhibitory avoidance task and tested for retention 24 h later. Post-training systemic injection of the bombesin/GRP receptor antagonist (D-Tpi6, Leu13 psi[CH2NH]-Leu14) bombesin (6-14) (RC-3095) impaired memory retention. In rats implanted under thionembutal anaesthesia with guide cannulae aimed at the BLA, post-training bilateral infusion of RC-3095 into the BLA dose-dependently impaired retention. Pre-training unilateral muscimol inactivation of the BLA blocked the memory-impairing effect of post-training systemic administration of RC-3095. The results suggest that bombesin/GRP receptors in the BLA are involved in the consolidation of aversive memory, and the BLA mediates the memory-impairing effect of systemic bombesin/GRP receptor blockade.