Biology:LYNX1
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Ly6/neurotoxin 1 is a protein in humans that is encoded by the LYNX1 gene.[1] Alternatively spliced variants encoding different isoforms have been identified.
Function
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 and Visual Plasticity
Transgenic mice without Lynx1 expression do not have a normal critical period of neuroplasticity in the visual cortex for development of ocular dominance columns.[4] 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.[2]
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]
References
- ↑ 1.0 1.1 "Entrez Gene: Ly6/neurotoxin 1". https://www.ncbi.nlm.nih.gov/sites/entrez?db=gene&cmd=retrieve&list_uids=66004.
- ↑ 2.0 2.1 2.2 "Optimizing cholinergic tone through lynx modulators of nicotinic receptors: implications for plasticity and nicotine addiction". Physiology 27 (4): 187–99. Aug 2012. doi:10.1152/physiol.00002.2012. PMID 22875450.
- ↑ "Manipulating neuronal circuits with endogenous and recombinant cell-surface tethered modulators". Frontiers in Molecular Neuroscience 2: 21. 2009. doi:10.3389/neuro.02.021.2009. PMID 19915728.
- ↑ "Neuroscience. Lynx for braking plasticity". Science 330 (6008): 1189–90. Nov 2010. doi:10.1126/science.1198983. PMID 21109660.
- ↑ 5.0 5.1 5.2 5.3 5.4 "Lynx1, a cholinergic brake, limits plasticity in adult visual cortex". Science 330 (6008): 1238–40. Nov 2010. doi:10.1126/science.1195320. PMID 21071629. Bibcode: 2010Sci...330.1238M.
This article incorporates text from the United States National Library of Medicine, which is in the public domain.
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