%0 Journal Article %T Lynx1 Prevents Long-Term Potentiation Blockade and Reduction of Neuromodulator Expression Caused by A¦Â1-42 and JNK Activation %A E. N. Lyukmanova %A M. A. Shulepko %A M. L. Bychkov %A M. P. Kirpichnikov %A N. A. Vasilyeva %A P. M. Balaban %J Archive of "Acta Naturae". %D 2018 %X Nicotinic acetylcholine receptors (nAChRs) are ligand-gated ion channels. Many neurodegenerative diseases are accompanied by cognitive impairment associated with the dysfunction of nAChRs. The human membrane-tethered prototoxin Lynx1 modulates nAChR function in the brain areas responsible for learning and memory. In this study, we have demonstrated for the first time that the ¦Â-amyloid peptide A¦Â1-42 decreases Lynx1 mRNA expression in rat primary cortical neurons, and that this decrease is associated with the activation of c-Jun N-terminal kinase (JNK). In addition, we have demonstrated that the Lynx1 expression decrease, as well as the blockade of the long-term potentiation underlying learning and memory, caused by A¦Â1-42, may be prevented by incubation with a water-soluble Lynx1 analogue. Our findings suggest that the water-soluble Lynx1 analogue may be a promising agent for the improvement of cognitive deficits in neurodegenerative diseases %K nicotinic acetylcholine receptor %K cognitive impairment %K Alzheimer disease %K ¦Â-amyloid peptide %K Ly6/uPAR %U https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6209405/