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Perspectives on Neuroscience and Behavior

Individuals with schizophrenia have cortical hypofrontality and they also have over three times the prevalence of smoking than the average population. genome-wide association studies have found single nucleotide polymorphisms (SNPs) in the human CHRNA5 gene (which encodes the alpha 5 nicotinic acetylcholine receptor [naCHR] subunit) that increase the risk for both smoking and schizophrenia. Now, it has been shown that mice that express a human alpha 5 subunit SNP (that results in partial loss of function of the alpha 5 naCHRs) have impaired social interaction and sensorimotor gating and decreased prelimbic prefrontal cortex layer II/III pyramidal cell activity. This involved layer II/III hierarchical inhibitory circuits where decreased activity of alpha 5 naCHR subunit containing vasoactive intestinal polypeptide interneurons produced an increased somatostatin interneuron inhibitory drive on layer II/III pyramidal neurons. Chronic nicotine infusion in mice containing the alpha 5 subunit SNP reversed the decreased pyramidal cell activity. This was found to involve nicotine-induced desensitization of beta 2 naCHR subunit containing receptors on somatostatin interneurons (Koukouli and others 2017). This elegant study provides evidence for a possible genetic-physiologic basis of hypofrontality in schizophrenia and the mechanisms involved when patients smoke in an attempt to reverse it. Most important, these findings now open new therapeutic possibilities of modulating alpha 5 naCHR subunit function to reduce hypofrontality in patients. In addition, they demonstrate how nicotine increases cortical function, which emphasizes the need to utilize safer and more effective methods of delivering nicotine than smoking.