α7 Nicotinic Acetylcholine Receptors in the Treatment of Schizophrenia

Neurochemical dysfunction in treated and nontreated schizophrenia – a retrospective analysis of in vivo imaging studies

“…In particular, reduced nicotinic α7 acetylcholine (nACh) receptor binding in the cingulate, hippocampus, and thalamus (for review, see Hajós and Rogers, 2010), reduced muscarinic M 1 and M 4 acetylcholine (mACh) receptor binding in the prefrontal cortex and hippocampus (for review, see Bymaster et al, 2002), reduced histamine H1 receptor binding in the frontal cortex (for review, see Ito, 2004), as well as increased or decreased endocannabinoid CB1 receptor binding in the prefrontal cortex and increased endocannabinoid CB1 receptor binding in the cingulate (for review, see Ferretjans et al, 2012) have been implicated in the pathophysiology of SZ.…”

Hippocampal network dynamics in response to α7 nACh receptors activation in amyloid-β overproducing transgenic mice

“…A promising symptomatic treatment targets neuronal α7 nicotinic acetylcholine receptors (α7 nAChRs). Selective activation of α7 nAChRs has been reported to improve various cognitive functions including attention, spatial learning, working memory, and episodic memory in rodents and non-human primates (Bitner et al, 2007;Hajós and Rogers, 2010;Levin, 2012).…”

Stoichiometry for drug potentiation of a pentameric ion channel

“…α7 has been implicated in several neurodegenerative and neuropsychiatric disorders (7)(8)(9). As a result, it has emerged as a potential therapeutic target, and several α7-specific compounds have been identified (10)(11)(12)(13). Of these, PNU-120596 (PNU) has the most pronounced effect (14).…”