Alpha-3 beta-2 nicotinic receptor

The alpha-3 beta-2 nicotinic receptor, also known as the α3β2 receptor, is a type of nicotinic acetylcholine receptor, consisting of α3 and β2 subunits.

It occurs alongside the more common α3β4 nicotinic receptor in autonomic ganglia, and as an facilitatory presynaptic autoreceptor at the neuromuscular junction (NMJ). At the NMJ, it is involved in upregulation of ACh release during high-frequency stimulation. Nicotine, a component of tobacco, a common stimulate of the receptor has been found to increase the concentration of this receptor.[1] Blockage of this receptor in the presence of a partial postsynaptic neuromuscular block is thought to produce the characteristic tetanic fade caused by non-depolarizing neuromuscular blockers.[2]

The receptor is classified as an allosteric enzyme that is generally activated by the natural agonist acetylcholine, however it may also be activated by external agonists such as nicotine and blocked by toxins such as bungarus toxin 3.1.[3] The main role of the receptor is to allow the re uptake of the neurotransmitter acetylcholine. Because it is a receptor involved in mechanisms including the neurotransmitter acetylcholine it is synthesized in the brain. However, α3β2 receptors synthesized in different locations of the brain may have differing regulatory properties. this is due to the cytoplasmic region in which the receptor is being formulated. Even though, there have been theories, how the increase in the receptors and uptaking of acetylcholine because of smoking nicotine can cause schizophrenia, no real correlation has been deducted. [4]

Ligands

Agonists

PAMs

Antagonists

See also

References

  1. ^ Buisson, Bruno; Bertrand, Daniel (2001-03-15). "Chronic Exposure to Nicotine Upregulates the Human α4β2 Nicotinic Acetylcholine Receptor Function". Journal of Neuroscience. 21 (6): 1819–1829. doi:10.1523/JNEUROSCI.21-06-01819.2001. ISSN 0270-6474. PMC 6762627. PMID 11245666.
  2. ^ Fagerlund, M.J.; Eriksson, L.I. (2009). "Current concepts in neuromuscular transmission". British Journal of Anaesthesia. pp. 108–114. doi:10.1093/bja/aep150. PMID 19546202.
  3. ^ Boulter, Jim (November 1, 1987). "Functional Expression of Two Neuronal Nicotinic Acetylcholine Receptors from cDNA Clones Identifies a Gene Family". Proceedings of the National Academy of Sciences of the United States of America. 84 (21): 7763–7767. Bibcode:1987PNAS...84.7763B. doi:10.1073/pnas.84.21.7763. PMC 299381. PMID 2444984.
  4. ^ Faraone, Stephen (2004). "A Novel Permutation Testing Method Implicates Sixteen Nicotinic Acetylcholine Receptor Genes as Risk Factors for Smoking in Schizophrenia Families". Human Heredity. 57 (2): 59–68. doi:10.1159/000077543. PMID 15192278. S2CID 22174623.
  5. ^ a b c d e f g h i Chavez-Noriega LE, Gillespie A, Stauderman KA, et al. (October 2000). "Characterization of the recombinant human neuronal nicotinic acetylcholine receptors alpha3beta2 and alpha4beta2 stably expressed in HEK293 cells". Neuropharmacology. 39 (13): 2543–60. doi:10.1016/s0028-3908(00)00134-9. PMID 11044726. S2CID 53250782.
  6. ^ Mihalak KB, Carroll FI, Luetje CW (September 2006). "Varenicline is a partial agonist at alpha4beta2 and a full agonist at alpha7 neuronal nicotinic receptors". Mol. Pharmacol. 70 (3): 801–5. doi:10.1124/mol.106.025130. PMID 16766716. S2CID 14562170.
  7. ^ Levandoski MM, Piket B, Chang J (June 2003). "The anthelmintic levamisole is an allosteric modulator of human neuronal nicotinic acetylcholine receptors". Eur. J. Pharmacol. 471 (1): 9–20. doi:10.1016/s0014-2999(03)01796-5. PMID 12809947.
  8. ^ Seo S, Henry JT, Lewis AH, Wang N, Levandoski MM (July 2009). "The positive allosteric modulator morantel binds at noncanonical subunit interfaces of neuronal nicotinic acetylcholine receptors". J. Neurosci. 29 (27): 8734–42. doi:10.1523/JNEUROSCI.1859-09.2009. PMC 2726771. PMID 19587280.
  9. ^ Crooks PA, Bardo MT, Dwoskin LP (2014). "Nicotinic Receptor Antagonists as Treatments for Nicotine Abuse". Emerging Targets & Therapeutics in the Treatment of Psychostimulant Abuse. Advances in Pharmacology. Vol. 69. pp. 513–51. doi:10.1016/B978-0-12-420118-7.00013-5. ISBN 9780124201187. PMC 4110698. PMID 24484986.
  10. ^ Lee RH, Tseng TY, Wu CY, et al. (2012). "Memantine inhibits α3β2-nAChRs-mediated nitrergic neurogenic vasodilation in porcine basilar arteries". PLOS ONE. 7 (7): e40326. Bibcode:2012PLoSO...740326L. doi:10.1371/journal.pone.0040326. PMC 3390354. PMID 22792283.
  11. ^ Hone AJ, Fisher F, Christensen S, Gajewiak J, Larkin D, Whiteaker P, McIntosh JM (July 2019). "PeIA-5466: A Novel Peptide Antagonist Containing Non-natural Amino Acids That Selectively Targets α3β2 Nicotinic Acetylcholine Receptors". Journal of Medicinal Chemistry. 62 (13): 6262–6275. doi:10.1021/acs.jmedchem.9b00566. PMC 7342494. PMID 31194549.


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