作者: Grazyna Biala , Marta Kruk-Slomka , Krzysztof Jozwiak
DOI: 10.1007/S00210-013-0866-Z
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摘要: Nicotinic cholinergic receptors (nAChRs) form a heterogeneous family of ligand-gated ion channels found in the nervous system. The main objective our research was to investigate interaction between nicotinic system and calcium homeostasis cognitive processes using modified elevated plus maze memory model mice. time each mouse took move from open arm either enclosed arms on retention trial (transfer latency, TL2) used as an index memory. Our results showed that single injection nicotine (0.035 0.175 mg/kg) shortened TL2 values, improving memory-related processes. Similarly, L-type channel antagonists (CCAs), i.e., flunarizine, verapamil, amlodipine, nimodipine, nifedipine, nicardipine (at range dose 5–20 mg/kg) administered before or after training, decreased value acquisition and/or consolidation. Interestingly, at subthresold doses, nicardipine, bupropion, nAChR antagonist, significantly reversed improvement acquisition, while bupropion attenuated consolidation provoked by acute (0.035 mg/kg, s.c.). After subchronic administration (14 days, i.p.) verapamil two CCAs with highest affinity for nAChRs, only (5 mg/kg) impaired both subthresold, ineffective (2.5 mg/kg), findings can be useful better understand calcium-related mechanisms