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DeutschHeteroreceptor
A heteroreceptor is a receptor located in the cell membrane of a neuron, regulating the synthesis and/or the release of mediators other than its own ligand.[1]These receptors play a crucial role in modulating neurotransmitter systems and are often targets for therapeutic drugs. By influencing the activity of other neurotransmitters, heteroreceptors contribute to the complex regulation of neural communication and have been implicated in various physiological and pathological processes.[2]
Heteroreceptors may be located in any part of the Neuron including the dendrites, the cell body, the axon, or the axon terminals.
Heteroreceptors respond to neurotransmitters, neuromodulators, or neurohormones released from adjacent neurons or cells; they are opposite to autoreceptors, which are sensitive only to neurotransmitters or hormones released by the cell in whose wall they are embedded.[3]
Examples
[edit]- Norepinephrine can influence the release of acetylcholine from parasympathetic neurons by acting on α2 adrenergic (α2A, α2B, and α2C) heteroreceptors.[4]These effects are related to analgesia, sedation, hypothermia.[5]
- DA D1 like heteroreceptors (D1 and D5) boost excitability and enhance NMDA receptor and calcium channel activity, while DA D2-like receptors (D2, D3, and D4) activate GIRK channels to help regulate movement, thinking, and motivation.[6]
- Acetylcholine can influence the release of norepinephrine from sympathetic neurons by acting on muscarinic-2 and muscarinic-4 heteroreceptors.
- CB1 negatively modulates the release of GABA[7][8] and glutamate,[9] playing a crucial role in maintaining a homeostasis between excitatory and inhibitory transmission.
- Glutamate released from an excitatory neuron escapes from the synaptic cleft and preferentially affects mGluR III receptors on the presynaptic terminals of interneurons. Glutamate spillover leads to inhibition of GABA release, modulating GABAergic transmission.[10][11]
See also
[edit]References
[edit]- ^ Laduron, Pierre M. (February 1985). "Presynaptic heteroreceptors in regulation of neuronal transmission". Biochemical Pharmacology. 34 (4): 467–470. doi:10.1016/0006-2952(85)90176-5. PMID 2578794.
- ^ Fuxe, Kjell; Borroto-Escuela, Dasiel O. (2016-01-01). "Heteroreceptor Complexes and their Allosteric Receptor–Receptor Interactions as a Novel Biological Principle for Integration of Communication in the CNS: Targets for Drug Development". Neuropsychopharmacology. 41 (1): 380–382. doi:10.1038/npp.2015.244. ISSN 1740-634X. PMC 4677137. PMID 26657959.
- ^ Schlicker, E.; Malinowska, B.; Kathmann, M.; Göthert, M. (1994-03-04). "Modulation of neurotransmitter release via histamine H 3 heteroreceptors". Fundamental & Clinical Pharmacology. 8 (2): 128–137. doi:10.1111/j.1472-8206.1994.tb00789.x. ISSN 0767-3981.
- ^ Ma, D.; Rajakumaraswamy, N.; Maze, M. (2004). "2-Adrenoceptor agonists: Shedding light on neuroprotection?". British Medical Bulletin. 71: 77–92. doi:10.1093/bmb/ldh036. PMID 15684247.
- ^ Gilsbach, Ralf; Hein, Lutz (January 2012). "Are the pharmacology and physiology of α 2 adrenoceptors determined by α 2 -heteroreceptors and autoreceptors respectively?". British Journal of Pharmacology. 165 (1): 90–102. doi:10.1111/j.1476-5381.2011.01533.x. ISSN 0007-1188. PMC 3252969. PMID 21658028.
- ^ Gawade, Shivaji Prataprao (2022-03-16). "Perspectives of Presynaptic Autoreceptors and Presynaptic Heteroreceptors in the Mechanism of Neurotransmission". Indian Journal of Pharmaceutical Education and Research. 56 (2): 329–346. doi:10.5530/ijper.56.2.53.
- ^ Katona, I.; Sperlágh, B.; Sík, A.; Käfalvi, A.; Vizi, E. S.; MacKie, K.; Freund, T. F. (1999). "Presynaptically located CB1 cannabinoid receptors regulate GABA release from axon terminals of specific hippocampal interneurons". The Journal of Neuroscience. 19 (11): 4544–4558. doi:10.1523/JNEUROSCI.19-11-04544.1999. PMC 6782612. PMID 10341254.
- ^ Sousa, V. C.; Assaife-Lopes, N. L.; Ribeiro, J. A.; Pratt, J. A.; Brett, R. R.; Sebastião, A. M. (2010). "Regulation of Hippocampal Cannabinoid CB1 Receptor Actions by Adenosine A1 Receptors and Chronic Caffeine Administration: Implications for the Effects of Δ9-Tetrahydrocannabinol on Spatial Memory". Neuropsychopharmacology. 36 (2): 472–487. doi:10.1038/npp.2010.179. PMC 3055664. PMID 20927050.
- ^ Hoffman, A. F.; Laaris, N.; Kawamura, M.; Masino, S. A.; Lupica, C. R. (2010). "Control of Cannabinoid CB1 Receptor Function on Glutamate Axon Terminals by Endogenous Adenosine Acting at A1 Receptors". Journal of Neuroscience. 30 (2): 545–555. doi:10.1523/JNEUROSCI.4920-09.2010. PMC 2855550. PMID 20071517.
- ^ Semyanov, A; Kullmann, D. M. (2000). "Modulation of GABAergic signaling among interneurons by metabotropic glutamate receptors". Neuron. 25 (3): 663–72. doi:10.1016/s0896-6273(00)81068-5. PMID 10774733.
- ^ Kullmann, D. M.; Semyanov, A (2002). "Glutamatergic modulation of GABAergic signaling among hippocampal interneurons: Novel mechanisms regulating hippocampal excitability". Epilepsia. 43 (Suppl 5): 174–8. doi:10.1046/j.1528-1157.43.s.5.12.x. PMID 12121316. S2CID 19781597.
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