作者: Kent T. Keyser , Christianne E. Strang , Kady S. Bruce , Barbara J. Morley , Marci L. Smith
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摘要: Purpose The α7 nicotinic acetylcholine receptor (nAChR) is widely expressed in the nervous system, including inner retinal neurons all species studied to date. Although reductions expression of nAChRs are thought contribute memory and visual deficits reported Alzheimer’s disease (AD) schizophrenia , nAChR knockout (KO) mouse viable has only slight dysfunction. The absence a major phenotypic abnormality may be attributable developmental mechanisms that serve compensate for loss. We hypothesized upregulation genes encoding other subunits or muscarinic (mAChR) subtypes during development partially accounts deficiencies KO mouse. purpose this study was determine whether deletion subunit model resulted changes regulation cholinergic receptors ion channels an when compared wild-type (WT)