PubMed · 1013258
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W W Moyer. 1976. Countercontrol in hypnotic control groups.. https://doi.org/10.2466/pr0.1976.39.3f.1083
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The selective sigma1 receptor agonist 1-(3,4-dimethoxyphenethyl)-4-(3-phenyl propyl)piperazine dihydrochloride (SA4503) was reported to reverse the amnesia induced by the muscarinic receptor antagonist scopolamine at sub-mg/kg doses. We examined its effect on the learning impairment induced in mice by the non-competitive NMDA receptor antagonist dizocilpine. Learning capacities were evaluated using spontaneous alternation in the Y-maze for spatial working memory, and step-down type passive avoidance. SA4503 (0.03-1 mg/kg s.c.) attenuated the dizocilpine (0.15 mg/kg i.p.)-induced memory deficits following a bell-shaped curve in both tests. These effects of SA4503 were blocked by haloperidol (0.05 mg/kg i.p.), implicating sigma1 receptors. SA4503 also reversed the alternation deficit induced by N(omega)-nitro-L-arginine methyl ester (L-NAME, 100 mg/kg i.p.) at the same dosage, indicating that it acted on working memory through the nitric oxide (NO)-mediated signalling pathway. Furthermore, progesterone (2 mg/kg s.c.) blocked the SA4503 effects in the dizocilpine- and L-NAME-amnesia models, in accordance with the purported neurosteroids/sigma1 receptors interaction. These results demonstrate a promising neurobehavioural profile of SA4503, a ligand equally efficient to reverse the deficit in the glutamatergic as well as in the cholinergic amnesia model. Pertinent informations on the potential mechanism of the anti-amnesic effects of sigma1 receptor ligands were also obtained.
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Male Sprague-Dawley rats were injected (i.p.) with either midazolam (MDZ, 2.0 mg/kg) or vehicle (1.0 ml/kg) 10 min before they were trained on a multiple-trial inhibitory avoidance task. Immediately following the training, bicuculline methiodide (BMI; 2.0, 5.6, 56.0 or 197.0 pmol/0.5 microl) or vehicle (0.5 microl) was infused bilaterally into the amygdala. On a 48 h retention test the performance of the MDZ-treated animals was significantly poorer than that of controls. The retention of MDZ-treated animals given intra-amygdala injections of the lowest dose of BMI (2.0 pmol) was comparable to that of controls, whereas higher doses of BMI impaired retention. The present results are consistent with other findings indicating that the amygdala mediates the amnestic effects of benzodiazepines on aversive learning. Furthermore, these data suggest that benzodiazepines impair memory by disrupting post-training processes underlying memory consolidation.