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Available structures
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Aliases LYNX1, SLURP2, Ly6/neurotoxin 1
External IDs MGI: 1345180 HomoloGene: 8026 GeneCards: LYNX1
Species Human Mouse
RefSeq (mRNA)



RefSeq (protein)



Location (UCSC) Chr 8: 142.76 – 142.78 Mb Chr 15: 74.75 – 74.75 Mb
PubMed search [1] [2]
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Ly6/neurotoxin 1 is a protein in humans that is encoded by the LYNX1 gene.[3] 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.[3]

The LYNX1 gene codes for a protein (Lynx1) that binds to acetylcholine receptors in the brain.[4] Lynx1 a member of the Ly6 superfamily of proteins that are capable of modulating neurotransmitter receptors.[5]

Lynx1 and Visual Plasticity[edit]

Transgenic mice without Lynx1 expression do not have a normal critical period of neuroplasticity in the visual cortex for development of ocular dominance columns.[6] These mice show unusually rapid recovery from amblyopia in adulthood indicating a role in reduction of synaptic plasticity during the normal expression of Lynx1 in adult brain.[4]

Lynx1 reduces adult visual cortex plasticity by binding to nicotinic acetylcholine receptors (NAchR) and diminishing acetylcholine signaling.[7] 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).[7] Lynx1 and nAChR mRNAs are co-expressed in the LGN, as well as in parvalbumin-positive GABAergic interneurons.[7] 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.[7] Similarly, an infusion of physostigmine to increase acetylcholine signaling prompted recovery from amblyopia in wild type mice[7] 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[edit]

Other Ly6 family proteins that are expressed in the brain: Lynx2, LYPD6, LYPD6B and PSCA.[4]


  1. ^ "Human PubMed Reference:". 
  2. ^ "Mouse PubMed Reference:". 
  3. ^ a b "Entrez Gene: Ly6/neurotoxin 1". 
  4. ^ a b c Miwa 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. PMID 22875450. 
  5. ^ Holford M, Auer S, Laqua M, Ibañez-Tallon I (2009). "Manipulating neuronal circuits with endogenous and recombinant cell-surface tethered modulators". Frontiers in Molecular Neuroscience. 2: 21. doi:10.3389/neuro.02.021.2009. PMC 2776481Freely accessible. PMID 19915728. 
  6. ^ Higley MJ, Strittmatter SM (Nov 2010). "Neuroscience. Lynx for braking plasticity". Science. 330 (6008): 1189–90. doi:10.1126/science.1198983. PMC 3244692Freely accessible. PMID 21109660. 
  7. ^ a b c d e Morishita H, Miwa JM, Heintz N, Hensch TK (Nov 2010). "Lynx1, a cholinergic brake, limits plasticity in adult visual cortex". Science. 330 (6008): 1238–40. doi:10.1126/science.1195320. PMC 3387538Freely accessible. PMID 21071629. 

This article incorporates text from the United States National Library of Medicine, which is in the public domain.