Abstract. We investigated the participation of γ-aminobutyric acid (GABA) neurons of the medial septal area in eight-arm radial maze performance in rats. The intra-septal injection of muscimol, a GABA A agonist, caused an increase in total error and working memory error. On the other hand, no significant effect was observed with reference memory error. Donepezil and tacrine (cholinesterase inhibitors) antagonized the muscimol-induced spatial memory deficits. Histidine (1500 mg / kg, i.p.) also improved the total error and working memory error induced by muscimol. At this dose, histidine caused a significant increase in the histamine content of the cortex, hippocampus, and hypothalamus in rats. In addition, the intra-hippocampal injection of histamine also antagonized muscimol-induced spatial memory deficits. The practical conclusion is that the GABA A receptor of the medial septal area plays an important role in working memory, and also, the disturbance of working memory induced by muscimol is mediated not only by cholinergic but also by histaminergic systems in the spatial memory of rats.

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Abstract. Triazolam caused no significant increase in the total error at 0.05 and 0.1 mg / kg. However, at 0.2 mg / kg, it caused a significant increase in total error. Almost the same findings were observed with brotizolam and rilmazafone. That is, at 0.2 and 0.5 mg / kg of brotizolam, 0.5 and 1.0 mg / kg of rilmazafone caused no significant increase in the total error. However, brotizolam at 1.0 mg / kg and rilmazafone at 2.0 mg / kg caused a significant increase in total error. Triazolam (0.05 mg / kg) and ethanol (1.0 g / kg) showed no significant effect on the numbers of errors when used alone separately, but the simultaneous use of triazolam and ethanol caused a significant increase in total error. Almost the same findings were observed with the coadministration of brotizolam (0.2 mg / kg) or rilmazafone (0.5 mg / kg) with ethanol. These results clearly indicate that all the short-acting benzodiazepines used in the study showed potentiation by ethanol in spatial memory deficits in mice.

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Abstract. The effect of [pGlu 4 ,Cyt 6 ,Arg 8 ]-vasopressin fragment 4-9 (AVP4-9) on group I metabotropic glutamate (mGlu 1 ) receptor antagonist-induced memory deficits was studied using 8-arm radial maze performance with 4 arms baited. In addition, the participation of the cholinergic system in the ameliorating effect of AVP4-9 on mGlu 1 receptor antagonist-induced memory deficits was also investigated. Intrahippocampal injection of (R,S)-1-aminoindan-1,5-dicarboxylic acid (AIDA), an mGlu 1 -receptor antagonist, significantly increased total error, reference memory error, and working memory error at a dose of 20 nmol / side. AVP4-9 (0.1 and 1.0 μg/ kg, s.c.) showed a significant ameliorative effect on AIDA-induced memory deficits. Improvement of AIDA-induced memory deficit in response to AVP4-9 treatment was significantly antagonized by scopolamine (5 nmol / side) but not by mecamylamine (200 nmol / side) at a dose that caused no effect on performance when injected separately. These findings indicate that the ameliorating effect of AVP4-9 on AIDA-induced memory deficit may be closely associated with the muscarinic receptor.