Ly6/neurotoxin 1 is a protein in humans that is encoded by the LYNX1gene.[1]Alternatively spliced variants encoding different isoforms have been identified.
This gene encodes a member of the Ly-6/neurotoxin gene family, a group of lymphocyte antigens that attach to the cell surface by a glycosylphosphatidylinositol anchor and have a unique structure showing conserved 8-10 cysteine residues with a characteristic spacing pattern. Functional analysis indicates that this protein is not a ligand or neurotransmitter but has the capacity to enhance nicotinic acetylcholine receptor function in the presence of acetylcholine. This gene may also play a role in the pathogenesis of psoriasis vulgaris.[1]
The LYNX1 gene codes for a protein (Lynx1) that binds to acetylcholine receptors in the brain.[2] Lynx1 a member of the Ly6 superfamily of proteins that are capable of modulating neurotransmitter receptors.[3]
Lynx1 reduces adult visual cortex plasticity by binding to nicotinic acetylcholine receptors (NAchR) and diminishing acetylcholine signaling.[5] After the developmental critical period and into adulthood, both Lynx1 mRNA and protein levels increase in the adult V1 and the lateral geniculate nucleus (LGN).[5] Lynx1 and nAChR mRNAs are co-expressed in the LGN, as well as in parvalbumin-positive GABAergic interneurons.[5] After monocular deprivation during the critical period to induce amblyopia, Lynx1 knock-out rat models spontaneously recovered normal visual acuity by reopening the closed eye.[5] Similarly, an infusion of physostigmine to increase acetylcholine signaling prompted recovery from amblyopia in wild type mice[5] Inhibition of Lynx1 may be a possible therapeutic mechanism to prolong synaptic plasticity of the visual cortex and improve binocular function of some amblyopes.
See also
Other Ly6 family proteins that are expressed in the brain: Lynx2, LYPD6, LYPD6B and PSCA.[2]
↑ 2.02.12.2Miwa JM, Lester HA, Walz A (Aug 2012). "Optimizing cholinergic tone through lynx modulators of nicotinic receptors: implications for plasticity and nicotine addiction". Physiology. 27 (4): 187–99. doi:10.1152/physiol.00002.2012. PMID22875450.