Endogenous benzodiazepine modulation of memory processes.
The immediate posttraining administration of the GABA antagonist, bicuculline, or of the Cl-channel blockers, picrotoxin or Ro 5-4864, enhances memory. These drugs are effective when injected into the amygdaloid nucleus. Intraamygdala muscimol has an opposite effect. All this suggests that memory is modulated at the posttraining period by GABA-A receptors. The pre-, but not posttraining systemic administration of benzodiazepines hinders, and that of inverse agonists, or of the benzodiazepine antagonist, flumazenil enhances retention of diverse tasks. Flumazenil, at doses lower than those that cause an enhancement, antagonizes the effect of benzodiazepine agonists and inverse agonists. This suggests that memory is modulated during acquisition by endogenous benzodiazepine receptor ligands: possibly the diazepam that was recently discovered in brain. Pretraining intraamygdala muscimol administration depresses memory, at doses several times higher than those that are effective posttraining. Pretraining Ro 5-4864 has no effect. This suggests that the release of endogenous benzodiazepines during training may modulate a GABA-A receptor complex, possibly in the amygdala, making it more sensitive to muscimol or Ro 5-4864 in the immediate posttraining period.[1]References
- Endogenous benzodiazepine modulation of memory processes. Izquierdo, I., Cunha, C., Medina, J.H. Neuroscience and biobehavioral reviews. (1990) [Pubmed]
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