title: The mitochondrial benzodiazepine receptor and avoidance learning in the day-old chick.
abstract: The specific mitochondrial benzodiazepine receptor (MBR) agonist, FGIN 1-27, and antagonist, PK 11195, were used to investigate whether this receptor was involved in passive avoidance memory formation in the day-old chick. PK 11195 at a concentration of 1-10 microM was found to be amnesic when injected directly into the lobus parolfactorius (LPO) 5 h after training (P<.01). Unilateral injections of PK 11195 further showed that memory was only disrupted with injections into the right hemisphere (P<.01). Since the MBR is considered to be involved in the production of a neurosteroid that modulates GABAergic transmission, we injected bicuculline and muscimol, specific inhibitor and agonist, respectively, of the GABA(A) receptor, to see if either disrupted memory formation. The results of bilateral injections into the LPO at 5 h post-training indicated that enhanced GABAergic transmission was involved in memory formation since the inhibitor, bicuculline, caused amnesia (P<.01) and unilateral injections also showed that this effect was confined to the right hemisphere (P<.05). Since memory for passive avoidance learning is thought to involve both cytosolic and mitochondrial protein synthesis at this 5-h time point [Freeman FM, Young IG. Chloramphenicol-induced amnesia for passive avoidance training in the day-old chick. Neurobiol Learn Mem 1999;71:80-93.], we studied the effect of unilateral injections of chloramphenicol (CAP) and anisomycin (ANI) during this second wave of protein synthesis and found that CAP only disrupted memory when injected into the right LPO 5 h post-training (P<.05). This lateralization to the right hemisphere was also seen when ANI was injected 4 h post-training (P<.05) but at 5 h, only bilateral injections of ANI could disrupt memory (P<.05). The results suggest a role for mitochondria and the GABAergic system in the retention of passive avoidance learning in the day-old chick.
authors: Division of Biochemistry and Molecular Biology, John Curtin School of Medical Research, The Australian National University, ACT 0200, Canberra, Australia.
authors: F M
authors: FM
authors: Freeman
authors: I G
authors: IG
authors: Young
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D000841:Anisomycin / Q000494:pharmacology; D001362:Avoidance Learning / Q000187:drug effects / Q000502:physiology*; D001640:Bicuculline / Q000494:pharmacology; D002645:Chickens; D002701:Chloramphenicol / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D005260:Female; D018755:GABA Agonists / Q000494:pharmacology; D018756:GABA Antagonists / Q000494:pharmacology; D058785:GABA-A Receptor Agonists; D058787:GABA-A Receptor Antagonists; D007210:Indoleacetic Acids / Q000494:pharmacology; D007267:Injections / Q000379:methods; D007546:Isoquinolines / Q000494:pharmacology; D008297:Male; D008568:Memory / Q000187:drug effects; D008928:Mitochondria / Q000378:metabolism*; D009118:Muscimol / Q000494:pharmacology; D016548:Prosencephalon / Q000187:drug effects / Q000502:physiology; D011500:Protein Synthesis Inhibitors / Q000494:pharmacology; D011963:Receptors, GABA-A / Q000502:physiology*
chemical_list: D018755:GABA Agonists; D018756:GABA Antagonists; D058785:GABA-A Receptor Agonists; D058787:GABA-A Receptor Antagonists; D007210:Indoleacetic Acids; D007546:Isoquinolines; D011500:Protein Synthesis Inhibitors; D011963:Receptors, GABA-A; C081306:N,N-di-n-hexyl-2-(4-fluorophenyl)indole-3-acetamide; D009118:Muscimol; D002701:Chloramphenicol; D000841:Anisomycin; D001640:Bicuculline; C037850:PK 11195