A publication in Nature Medicine by Boris Gutkin and his colleagues.

We are very pleased to congratulate our colleague Boris Gutkin with publication in Nature Medicine, entitled: "Nicotine reverses hypofrontality in animal models of addiction and schizophrenia".

Boris Gutkin, PhD is a head of Theoretical Neuroscience Group here at HSE as well as a member of Group of Neural Theory in Ecole Normale Supérieure, Paris, France. See below an abstract of the paper together with additional information.

"The prefrontal cortex (PFC) underlies higher cognitive processes¹ that are modulated by nicotinic acetylcholine receptor (nAChR) activation by cholinergic inputs². PFC spontaneous default activity³ is altered in neuropsychiatric disorders⁴, including schizophrenia⁵—a disorder that can be accompanied by heavy smoking⁶. Recently, genome-wide association studies (GWAS) identified single-nucleotide polymorphisms (SNPs) in the human  CHRNA5  gene, encoding the  α 5 nAChR subunit, that increase the risks for both smoking and schizophrenia^7, 8. Mice with altered nAChR gene function exhibit PFC-dependent behavioral deficits^9, 10, 11, but it is unknown how the corresponding human polymorphisms alter the cellular and circuit mechanisms underlying behavior. Here we show that mice expressing a human  α 5 SNP exhibit neurocognitive behavioral deficits in social interaction and sensorimotor gating tasks. Two-photon calcium imaging in awake mouse models showed that nicotine can differentially influence PFC pyramidal cell activity by nAChR modulation of layer II/III hierarchical inhibitory circuits. In  α 5-SNP-expressing and  α 5-knockout mice, lower activity of vasoactive intestinal polypeptide (VIP) interneurons resulted in an increased somatostatin (SOM) interneuron inhibitory drive over layer II/III pyramidal neurons. The decreased activity observed in  α 5-SNP-expressing mice resembles the hypofrontality observed in patients with psychiatric disorders, including schizophrenia and addiction^5, 12. Chronic nicotine administration reversed this hypofrontality, suggesting that administration of nicotine may represent a therapeutic strategy for the treatment of schizophrenia, and a physiological basis for the tendency of patients with schizophrenia to self-medicate by smoking¹³."

Link to the article: http://www.nature.com/nm/journal/vaop/ncurrent/full/nm.4274.html