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Publication : Deficits of synaptic functions in hippocampal slices prepared from aged mice null α7 nicotinic acetylcholine receptors.

First Author  Ma L Year  2014
Journal  Neurosci Lett Volume  570
Pages  97-101 PubMed ID  24769321
Mgi Jnum  J:214007 Mgi Id  MGI:5587862
Doi  10.1016/j.neulet.2014.04.018 Citation  Ma L, et al. (2014) Deficits of synaptic functions in hippocampal slices prepared from aged mice null alpha7 nicotinic acetylcholine receptors. Neurosci Lett 570:97-101
abstractText  Alpha 7 (alpha7) nicotinic acetylcholine receptor (alpha7-nAChR) is one of most high expressed nAChR subtypes in the brain. The activation of nAChRs enhances animal cognitive, learning and memory abilities. However, the role of genetic knockout (KO) of alpha7-nAChRs in animal cognition-associated behaviors is still obscure. An early report showed that alpha7-nAChR KO mice did not exhibit behavioral phenotypes, concerning the roles of alpha7-nAChRs in normal, cognition-associated behaviors. Later, alpha7-nAChR KO mice were found a deficit in animal spatial discrimination. The roles of alpha7-nAChRs in the alterations of hippocampal synaptic function during aging process are largely unknown. Here, we address this question by examining synaptic function using field potential recording in hippocampal slice preparations from adult (12-14 months old) and aged (22-24 months old) alpha7-nAChR KO and age-matched wild-type (WT) mice. We found that compared to aged WT mice, aged alpha7-nAChR KO mice exhibited significantly reduced size of evoked field synaptic potential and impaired long-term potentiation (LTP) in hippocampal CA3-CA1 synapses. However, adult alpha7-nAChR KO mice did not show a clear deficit in LTP although the basic synaptic transmission was also reduced compared to adult WT mice. In both age groups, there was no significant difference of paired-pulse facilitation between alpha7-nAChR KO and WT mice. Collectively, this study provides direct evidence, for the first time, that the impaired synaptic function occurs in aged alpha7-nAChR KO mice, suggesting an importance of alpha7-nAChRs in maintaining cognitive function during aging process.
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