Ly6/neurotoxin 1 is a protein in humans that is encoded by the LYNX1 gene. [5] Alternatively spliced variants encoding different isoforms have been identified.
Ly6/neurotoxin 1 is a protein in humans that is encoded by the LYNX1 gene. [5] 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. [5]
The LYNX1 gene codes for a protein (Lynx1) that binds to acetylcholine receptors in the brain. [6] Lynx1 a member of the Ly6 superfamily of proteins that are capable of modulating neurotransmitter receptors. [7]
Transgenic mice without Lynx1 expression do not have a normal critical period of neuroplasticity in the visual cortex for development of ocular dominance columns. [8] 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. [6]
Lynx1 reduces adult visual cortex plasticity by binding to nicotinic acetylcholine receptors (NAchR) and diminishing acetylcholine signaling. [9] 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). [9] Lynx1 and nAChR mRNAs are co-expressed in the LGN, as well as in parvalbumin-positive GABAergic interneurons. [9] 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. [9] Similarly, an infusion of physostigmine to increase acetylcholine signaling prompted recovery from amblyopia in wild type mice [9] Inhibition of Lynx1 may be a possible therapeutic mechanism to prolong synaptic plasticity of the visual cortex and improve binocular function of some amblyopes.
Other Ly6 family proteins that are expressed in the brain: Lynx2, LYPD6, LYPD6B and PSCA. [6]
Acetylcholine (ACh) is an organic chemical that functions in the brain and body of many types of animals as a neurotransmitter—a chemical message released by nerve cells to send signals to other cells, such as neurons, muscle cells and gland cells. Its name is derived from its chemical structure: it is an ester of acetic acid and choline. Parts in the body that use or are affected by acetylcholine are referred to as cholinergic. Substances that increase or decrease the overall activity of the cholinergic system are called cholinergics and anticholinergics, respectively.
An acetylcholine receptor is an integral membrane protein that responds to the binding of acetylcholine, a neurotransmitter.
In neurophysiology, long-term depression (LTD) is an activity-dependent reduction in the efficacy of neuronal synapses lasting hours or longer following a long patterned stimulus. LTD occurs in many areas of the CNS with varying mechanisms depending upon brain region and developmental progress.
A neuromuscular junction is a chemical synapse between a motor neuron and a muscle fiber. It allows the motor neuron to transmit a signal to the muscle fiber, causing muscle contraction.
Nicotinic acetylcholine receptors, or nAChRs, are receptor polypeptides that respond to the neurotransmitter acetylcholine. Nicotinic receptors also respond to drugs such as the agonist nicotine. They are found in the central and peripheral nervous system, muscle, and many other tissues of many organisms. At the neuromuscular junction they are the primary receptor in muscle for motor nerve-muscle communication that controls muscle contraction. In the peripheral nervous system: (1) they transmit outgoing signals from the presynaptic to the postsynaptic cells within the sympathetic and parasympathetic nervous system, and (2) they are the receptors found on skeletal muscle that receive acetylcholine released to signal for muscular contraction. In the immune system, nAChRs regulate inflammatory processes and signal through distinct intracellular pathways. In insects, the cholinergic system is limited to the central nervous system.
Muscarinic acetylcholine receptors, or mAChRs, are acetylcholine receptors that form G protein-coupled receptor complexes in the cell membranes of certain neurons and other cells. They play several roles, including acting as the main end-receptor stimulated by acetylcholine released from postganglionic fibers in the parasympathetic nervous system.
Synaptogenesis is the formation of synapses between neurons in the nervous system. Although it occurs throughout a healthy person's lifespan, an explosion of synapse formation occurs during early brain development, known as exuberant synaptogenesis. Synaptogenesis is particularly important during an individual's critical period, during which there is a certain degree of synaptic pruning due to competition for neural growth factors by neurons and synapses. Processes that are not used, or inhibited during their critical period will fail to develop normally later on in life.
Neuromodulation is the physiological process by which a given neuron uses one or more chemicals to regulate diverse populations of neurons. Neuromodulators typically bind to metabotropic, G-protein coupled receptors (GPCRs) to initiate a second messenger signaling cascade that induces a broad, long-lasting signal. This modulation can last for hundreds of milliseconds to several minutes. Some of the effects of neuromodulators include: alter intrinsic firing activity, increase or decrease voltage-dependent currents, alter synaptic efficacy, increase bursting activity and reconfiguration of synaptic connectivity.
The muscarinic acetylcholine receptor M4, also known as the cholinergic receptor, muscarinic 4 (CHRM4), is a protein that, in humans, is encoded by the CHRM4 gene.
Neuronal acetylcholine receptor subunit beta-2 is a protein that in humans is encoded by the CHRNB2 gene.
Neuronal acetylcholine receptor subunit alpha-3, also known as nAChRα3, is a protein that in humans is encoded by the CHRNA3 gene. The protein encoded by this gene is a subunit of certain nicotinic acetylcholine receptors (nAchR). Research with mecamylamine in animals has implicated alpha-3-containing nAChRs in the abusive and addictive properties of ethanol.
Neuronal acetylcholine receptor subunit alpha-5, also known as nAChRα5, is a protein that in humans is encoded by the CHRNA5 gene. The protein encoded by this gene is a subunit of certain nicotinic acetylcholine receptors (nAchR).
Neuronal acetylcholine receptor subunit alpha-2, also known as nAChRα2, is a protein that in humans is encoded by the CHRNA2 gene. The protein encoded by this gene is a subunit of certain nicotinic acetylcholine receptors (nAchR).
Neuronal acetylcholine receptor subunit alpha-9, also known as nAChRα9, is a protein that in humans is encoded by the CHRNA9 gene. The protein encoded by this gene is a subunit of certain nicotinic acetylcholine receptors (nAchR).
Ly6/PLAUR domain-containing protein 1 is a protein that in humans is encoded by the LYPD1 gene.
Cholinergic receptor, nicotinic, alpha 6, also known as nAChRα6, is a protein that in humans is encoded by the CHRNA6 gene. The CHRNA6 gene codes for the α6 nicotinic receptor subunit that is found in certain types of nicotinic acetylcholine receptors found primarily in the brain. Neural nicotinic acetylcholine receptors containing α6 subunits are expressed on dopamine-releasing neurons in the midbrain, and dopamine release following activation of these neurons is thought to be involved in the addictive properties of nicotine. Due to their selective localisation on dopaminergic neurons, α6-containing nACh receptors have also been suggested as a possible therapeutic target for the treatment of Parkinson's disease. In addition to nicotine, research in animals has implicated alpha-6-containing nAChRs in the abusive and addictive properties of ethanol, with mecamylamine demonstrating a potent ability to block these properties.
Neuronal acetylcholine receptor subunit alpha-10, also known as nAChRα10 and cholinergic receptor nicotinic alpha 10, is a protein that in humans is encoded by the CHRNA10 gene. The protein encoded by this gene is a subunit of certain nicotinic acetylcholine receptors (nAchR).
The LU domain is an evolutionally conserved protein domain of the three-finger protein superfamily. This domain is found in the extracellular domains of cell-surface receptors and in either GPI-anchored or secreted globular proteins, for example the Ly-6 family, CD59, and Sgp-2.
Three-finger proteins or three-finger protein domains are a protein superfamily consisting of small, roughly 60-80 amino acid residue protein domains with a common tertiary structure: three beta strand loops extended from a hydrophobic core stabilized by disulfide bonds. The family is named for the outstretched "fingers" of the three loops. Members of the family have no enzymatic activity, but are capable of forming protein-protein interactions with high specificity and affinity. The founding members of the family, also the best characterized by structure, are the three-finger toxins found in snake venom, which have a variety of pharmacological effects, most typically by disruption of cholinergic signaling. The family is also represented in non-toxic proteins, which have a wide taxonomic distribution; 3FP domains occur in the extracellular domains of some cell-surface receptors as well as in GPI-anchored and secreted globular proteins, usually involved in signaling.
LY6/PLAUR Domain Containing 6B, also known under the name Cancer/Testis Antigen 116 (CTA116) and LYPD7 is encoded by the LYPD6B gene. LYPD6B is a member of the lymphocyte antigen 6 (LY6) protein family. It is expressed in the testis, lungs, stomach and the prostate and in the nervous system where it acts as a modulator of nicotinic acetylcholine receptor activity.
This article incorporates text from the United States National Library of Medicine, which is in the public domain.