Article date: 1990/9/1
PubMed ID: 2173541
Journal name: Behavioral and neural biology (ISSN: 0163-1047)
In rats, amygdala benzodiazepine-like immunoreactivity decreases by 29% immediately after the animals step down from the platform of an inhibitory avoidance apparatus and decreases by a further 45% immediately after they receive a training footshock. The decrease is attributable to a release of diazepam or diazepam-like molecules. The immediate post-training intraamygdala injection of the central benzodiazepine antagonist flumazenil (10 nmole/amygdala) causes memory facilitation, and that of the GABA-A agonist muscimol (0.005 to 0.5 nmole) causes retrograde amnesia. Pretraining ip flumazenil administration (2.0 and 5.0 mg/kg) attenuates the effect of post-training muscimol by a factor of at least 100. The higher dose of pretraining flumazenil also causes memory facilitation. The data suggest that post-training consolidation is down-regulated by a GABA-A mechanism in the amygdala modulated by endogenous benzodiazepines released during training and at the time of consolidation.
Author List: Izquierdo I, Da Cunha C, Huang C H, Walz R, Wolfman C, Medina J H
Publication Types: Journal Article; Research Support, Non-U.S. Gov't
Substances mentioned in the article: Receptors, GABA-A; Benzodiazepines; Muscimol; Flumazenil;
Mesh terms: Amygdala/drug effects; Animals; Arousal/physiology; Avoidance Learning/drug effects; Benzodiazepines/metabolism; Dose-Response Relationship, Drug; Down-Regulation/physiology; Flumazenil/pharmacology; Male; Mental Recall/drug effects; Muscimol/pharmacology; Rats; Rats, Inbred Strains; Receptors, GABA-A/drug effects; Retention (Psychology)/drug effects;