5-HT_1A receptor

The serotonin 1A receptor (or 5-HT_1A receptor) is a subtype of serotonin receptor (5-HT receptor) that binds the neurotransmitter serotonin (5-hydroxytryptamine, 5-HT). It is a G protein-coupled receptor (GPCR), coupled to the Gi protein, that mediates inhibitory neurotransmission. The serotonin 1A receptor is encoded by the HTR1A gene.[5][6]

HTR1A
Identifiers
Aliases	HTR1A, 5-hydroxytryptamine (serotonin) receptor 1A, G protein-coupled, 5-HT-1A, 5-HT1A, 5HT1a, ADRB2RL1, ADRBRL1, G-21, PFMCD, 5-hydroxytryptamine receptor 1A
External IDs	OMIM: 109760 MGI: 96273 HomoloGene: 20148 GeneCards: HTR1A
Gene location (Human) Chr. Chromosome 5 (human)[1] Band 5q12.3 Start 63,960,356 bp[1] End 63,962,507 bp[1]
Gene location (Mouse) Chr. Chromosome 13 (mouse)[2] Band 13 D1|13 56.92 cM Start 105,443,639 bp[2] End 105,448,122 bp[2]
RNA expression pattern More reference expression data
Gene ontology Molecular function • G-protein coupled receptor activity • signal transducer activity • G-protein coupled serotonin receptor activity • GO:0001948 protein binding • serotonin binding • neurotransmitter receptor activity • receptor-receptor interaction Cellular component • integral component of membrane • membrane • cell membrane • integral component of plasma membrane • dendrite Biological process • G-protein coupled receptor signaling pathway • regulation of behavior • vasoconstriction • adenylate cyclase-inhibiting serotonin receptor signaling pathway • serotonin metabolic process • behavioral fear response • regulation of dopamine metabolic process • regulation of serotonin secretion • exploration behavior • serotonin receptor signaling pathway • positive regulation of cell proliferation • regulation of hormone secretion • cellular proliferation • signal transduction • animal behavior • G-protein coupled receptor signaling pathway, coupled to cyclic nucleotide second messenger • chemical synaptic transmission Sources:Amigo / QuickGO
Orthologs
Species	Human	Mouse
Entrez	3350	15550
Ensembl	ENSG00000178394	ENSMUSG00000021721
UniProt	P08908	Q64264
RefSeq (mRNA)	NM_000524	NM_008308
RefSeq (protein)	NP_000515	NP_032334
Location (UCSC)	Chr 5: 63.96 – 63.96 Mb	Chr 13: 105.44 – 105.45 Mb
PubMed search	[3]	[4]
Wikidata
View/Edit Human View/Edit Mouse

Distribution

The 5-HT_1A receptor is the most widespread of all the 5-HT receptors. In the central nervous system, 5-HT_1A receptors exist in the cerebral cortex, hippocampus, septum, amygdala, and raphe nucleus in high densities, while low amounts also exist in the basal ganglia and thalamus.[7][8][9] The 5-HT_1A receptors in the raphe nucleus are largely somatodendritic autoreceptors, whereas those in other areas such as the hippocampus are postsynaptic receptors.[8]

Function

Neuromodulation

5-HT_1A receptor agonists are involved in neuromodulation. They decrease blood pressure and heart rate via a central mechanism, by inducing peripheral vasodilation, and by stimulating the vagus nerve.[10] These effects are the result of activation of 5-HT_1A receptors within the rostral ventrolateral medulla.[10] The sympatholytic antihypertensive drug urapidil is an α₁-adrenergic receptor antagonist and 5-HT_1A receptor agonist, and it has been demonstrated that the latter property contributes to its overall therapeutic effects.[11][12] Vasodilation of the blood vessels in the skin via central 5-HT_1A activation increases heat dissipation from the organism out into the environment, causing a decrease in body temperature.[13][14]

Activation of central 5-HT_1A receptors triggers the release or inhibition of norepinephrine depending on species, presumably from the locus coeruleus, which then reduces or increases neuronal tone to the iris sphincter muscle by modulation of postsynaptic α₂-adrenergic receptors within the Edinger-Westphal nucleus, resulting in pupil dilation in rodents, and pupil constriction in primates including humans.[15][16][17]

5-HT_1A receptor agonists like buspirone[18] and flesinoxan[19] show efficacy in relieving anxiety[20] and depression,[21] and buspirone and tandospirone are currently approved for these indications in various parts of the world. Others such as gepirone,[22] flesinoxan,[19] flibanserin,[23] and naluzotan[24] have also been investigated, though none have been fully developed and approved yet. Some of the atypical antipsychotics like lurasidone[25] and aripiprazole[26] are also partial agonists at the 5-HT_1A receptor and are sometimes used in low doses as augmentations to standard antidepressants like the selective serotonin reuptake inhibitors (SSRIs).[27]

5-HT_1A autoreceptor desensitization and increased 5-HT_1A receptor postsynaptic activation via general increases in serotonin levels by serotonin precursor supplementation, serotonin reuptake inhibition, or monoamine oxidase inhibition has been shown to be a major mediator in the therapeutic benefits of most mainstream antidepressant supplements and pharmaceuticals, including serotonin precursors like L-tryptophan and 5-HTP, selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs), tricyclic antidepressants (TCAs), tetracyclic antidepressants (TeCAs), and monoamine oxidase inhibitors (MAOIs).[28] 5-HT_1A receptor activation likely plays a significant role in the positive effects of serotonin releasing agents (SRAs) like MDMA ("Ecstasy") as well.[29][30]

5-HT_1A receptors in the dorsal raphe nucleus are co-localized with neurokinin 1 (NK₁) receptors and have been shown to inhibit the release of substance P, their endogenous ligand.[31][32] In addition to being antidepressant and anxiolytic in effect, 5-HT_1A receptor activation has also been demonstrated to be antiemetic[33][34] and analgesic,[35][36] and all of these properties may be mediated in part or full, depending on the property in question, by NK₁ receptor inhibition. Consequently, novel NK₁ receptor antagonists are now in use for the treatment of nausea and emesis, and are also being investigated for the treatment of anxiety and depression.[37]

5-HT_1A receptor activation has been shown to increase dopamine release in the medial prefrontal cortex, striatum, and hippocampus, and may be useful for improving the symptoms of schizophrenia and Parkinson's disease.[38][39] As mentioned above, some of the atypical antipsychotics are 5-HT_1A receptor partial agonists, and this property has been shown to enhance their clinical efficacy.[38][40][41] Enhancement of dopamine release in these areas may also play a major role in the antidepressant and anxiolytic effects seen upon postsynaptic activation of the 5-HT_1A receptor.[42][43]

Activation of 5-HT_1A receptors has been demonstrated to impair certain aspects of memory (affecting declarative and non-declarative memory functions) and learning (due to interference with memory-encoding mechanisms), by inhibiting the release of glutamate and acetylcholine in various areas of the brain.[44] 5-HT_1A activation is known to improve cognitive functions associated with the prefrontal cortex, possibly via inducing prefrontal cortex dopamine and acetylcholine release.[45] Conversely, the 5-HT_1A antagonist, WAY100635, alleviated learning and memory impairments induced by glutamate blockade (with dizocilpine)[46] or hippocampal cholinergic denervation (by fornix transection)[47] in primates. Furthermore, 5-HT_1A receptor antagonists such as lecozotan have been shown to facilitate certain types of learning and memory in rodents, and as a result, are being developed as novel treatments for Alzheimer's disease.[48]

Other effects of 5-HT_1A activation that have been observed in scientific research include:

• Decreased aggression[49][50]
• Increased sociability[30]
• Decreased impulsivity[51]
• Inhibition of drug-seeking behavior[52][53][54]
• Facilitation of sex drive and arousal[55][56]
• Inhibition of penile erection[57][58]
• Diminished food intake[59]
• Prolongation of REM sleep latency[60][61]
• Reversal of opioid-induced respiratory depression[62]

Endocrinology

5-HT_1A receptor activation induces the secretion of various hormones including cortisol, corticosterone, adrenocorticotropic hormone (ACTH), oxytocin, prolactin, growth hormone, and β-endorphin.[63][64][65][66] The receptor does not affect vasopressin or renin secretion, unlike the 5-HT₂ receptors.[63][64] It has been suggested that oxytocin release may contribute to the prosocial, antiaggressive, and anxiolytic properties observed upon activation of the receptor.[30] β-Endorphin secretion may contribute to antidepressant, anxiolytic, and analgesic effects.[67]

Autoreceptors

5-HT_1A receptors can be located on the cell body, dendrites, axons, and both presynaptically and postsynaptically in nerve terminals or synapses. Those located on the soma and dendrites are referred to as somatodendritic, and those located presynaptically in the synapse are simply referred to as presynaptic. As a group, receptors that are sensitive to the neurotransmitter that is released by the neuron on which the receptors are located are known as autoreceptors; they typically constitute the key component of an ultra-short negative feedback loop whereby the neuron's release of neurotransmitter inhibits its further release of neurotransmitter. Stimulation of 5-HT_1A autoreceptors inhibits the release of serotonin in nerve terminals. For this reason, 5-HT_1A receptor agonists tend to exert a biphasic mode of action; they decrease serotonin release and postsynaptic 5-HT_1A receptor activity in low doses, and further decrease serotonin release but increase postsynaptic 5-HT_1A receptor activity at higher doses by directly stimulating the receptors in place of serotonin.

This autoreceptor-mediated inhibition of serotonin release has been theorized to be a major factor in the therapeutic lag that is seen with serotonergic antidepressants such as the SSRIs.[68] The autoreceptors must first desensitize before the concentration of extracellular serotonin in the synapse can become elevated appreciably.[68][69] Though the responsiveness of the autoreceptors is somewhat reduced with chronic treatment, they still remain effective at constraining large increases in extracellular serotonin concentrations.[68] For this reason, serotonin reuptake inhibitors that also have 5-HT_1A receptor antagonistic or partial agonistic properties, such as vilazodone and SB-649,915, are being investigated and introduced as novel antidepressants with the potential for a faster onset of action and improved effectiveness compared to those currently available.[70]

Unlike most drugs that elevate extracellular serotonin levels like the SSRIs and MAOIs, SRAs such as fenfluramine and MDMA bypass serotonin autoreceptors such as 5-HT_1A. They do this by directly acting on the release mechanisms of serotonin neurons and forcing release to occur regardless of autoreceptor-mediated inhibition.[71] As such, SRAs induce immediate and much greater increases in extracellular serotonin concentrations compared to other serotonin-elevating agents such as the SSRIs. In contrast to SRAs, SSRIs actually decrease serotonin levels initially and require several weeks of chronic dosing before serotonin concentrations reach their maximal elevation and full clinical benefits for conditions such as depression and anxiety are seen.[72][73] For these reasons, selective serotonin releasing agents (SSRAs) such as MDAI and MMAI have been proposed as novel antidepressants with a putatively faster onset of action and improved effectiveness compared to current treatments.[72]

Similarly to SRAs, sufficiently high doses of 5-HT_1A receptor agonists also bypass the 5-HT_1A autoreceptor-mediated inhibition of serotonin release and therefore increase 5-HT_1A postsynaptic receptor activation by directly agonizing the postsynaptic receptors in lieu of serotonin.

Ligands

The distribution of 5-HT_1A receptors in the human brain may be imaged with the positron emission tomography using the radioligand [¹¹C] WAY-100,635.[74] For example, one study has found increased 5-HT_1A binding in type 2 diabetes.[75] Another PET study found a negative correlation between the amount of 5-HT_1A binding in the raphe nuclei, hippocampus and neocortex and a self-reported tendency to have spiritual experiences.[76] Labeled with tritium, WAY-100,635 may also be used in autoradiography.[77]

Agonists

Partial agonists

• 2C-B[78]
• 2C-E[78]
• 2C-T-2[78]
• 4C-T-2[78]
• 5-CT
• 5-MT
• 5-MeO-DiPT[78]
• 5-MeO-DMT
• 5-MeO-MiPT[78]
• 5-MeO-TMT[78]
• 6-F-DMT[78]
• Adatanserin
• αET
• Amphetamine
• αMT
• Aripiprazole
• Asenapine
• Bacoside
• Bay R 1531
• Befiradol
• Binospirone
• Brexpiprazole
• Bufotenin
• Buspirone (postsynaptic 5HT1A)
• Cannabidiol[79]
• Cariprazine
• Clozapine
• Cis-2a[78]
• Dihydroergotamine
• Dimethyltryptamine
• DiPT[78]
• DOET[78]
• DOI[78]
• DPT[78]
• Ebalzotan
• Eltoprazine
• EMDT[78]
• Ergotamine
• Etoperidone
• F-11,461
• F-12,826
• F-13,714
• F-14,679
• Flesinoxan
• Flibanserin
• Ginkgo biloba[80]
• Gepirone
• Haloperidol
• Lamotrigine
• Ipsapirone
• Limonene
• Lisuride
• Lurasidone
• LY-301,317
• Lysergic acid diethylamide (LSD)
• Mescaline[78]
• 3,4-Methylenedioxyamphetamine[81]
• Methylphenidate
• Methysergide
• Naluzotan
• NBUMP
• Nefazodone
• Olanzapine
• Osemozotan (postsynaptic 5-HT_1A)
• Perospirone
• Pyrimidinylpiperazine
• Piclozotan
• Psilocin
• Psilocybin
• Quetiapine
• Rauwolscine
• RR-2B[78]
• RU-24,969
• S-15,535
• Sarizotan
• SS-2C[78]
• SSR-181,507
• Sunepitron
• Tandospirone
• Tiospirone
• Trazodone
• Trifluoromethylphenylpiperazine
• Trimethoxyamphetamine[78]
• Umespirone
• Urapidil
• Vilazodone
• Xaliproden
• Yohimbine
• Zalospirone
• Ziprasidone

Full agonists

• 8-OH-DPAT[82]
• Alnespirone
• Buspirone (presynaptic 5HT1A)
• Befiradol
• Eptapirone
• F-15,599
• Lesopitron
• MKC-242
• LY-293,284
• Osemozotan (presynaptic 5-HT_1A)
• Repinotan
• U-92,016-A
• Flibanserin
• Vortioxetine

Biased agonists

• HBK-17 – β-arrestin biased agonist[83]
• NLX-204 – ERK1/2 prefering agonist[84]

Antagonists

• Alprenolol
• AV-965
• Binospirone (postsynaptic 5-HT1A receptors)
• BMY-7,378
• Cyanopindolol
• Cyproheptadine
• Dotarizine
• Flopropione
• GR-46,611
• Iodocyanopindolol
• Isamoltane
• Lecozotan
• Mefway
• Methiothepin
• MPPF
• NAD-299
• NAN-190
• Nebivolol
• Oxprenolol
• Pindobind
• Pindolol
• Propranolol
• Risperidone
• Robalzotan
• SB-649,915
• SDZ-216,525
• Spiperone
• Spiramide
• Spiroxatrine
• UH-301
• WAY-100,135
• WAY-100,635
• Xylamidine

[85]

Genetics

The 5-HT_1A receptor is coded by the HTR1A gene. There are several human polymorphisms associated with this gene. A 2007 review listed 27 single nucleotide polymorphisms (SNP).[86] The most investigated SNPs are C-1019G (rs6295), C-1018G,[87] Ile28Val (rs1799921), Arg219Leu (rs1800044), and Gly22Ser (rs1799920).[86] Some of the other SNPs are Pro16Leu, Gly272Asp, and the synonymous polymorphism G294A (rs6294). These gene variants have been studied in relation to psychiatric disorders with no definitive results.[86]

Protein-protein interactions

The 5-HT_1A receptor has been shown to interact with brain-derived neurotrophic factor (BDNF), which may play a major role in its regulation of mood and anxiety.[88][89]

Receptor oligomers

The 5-HT_1A receptor forms heterodimers with the following receptors: 5-HT₇,[90] 5-HT_1B, 5-HT_1D, GABA_B2, GPCR26, LPA₁, LPA₃, S1P₁, S1P₃.[91]

See also

• 5-HT receptor
• 5-HT₁ receptor

References

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Further reading

• el Mestikawy S, Fargin A, Raymond JR, Gozlan H, Hnatowich M (1991). "The 5-HT1A receptor: an overview of recent advances". Neurochem. Res. 16 (1): 1–10. doi:10.1007/BF00965820. PMID 2052135.
• Hensler JG (2003). "Regulation of 5-HT1A receptor function in brain following agonist or antidepressant administration". Life Sci. 72 (15): 1665–82. doi:10.1016/S0024-3205(02)02482-7. PMID 12559389.
• Van Oekelen D, Luyten WH, Leysen JE (2003). "5-HT2A and 5-HT2C receptors and their atypical regulation properties". Life Sci. 72 (22): 2429–49. doi:10.1016/S0024-3205(03)00141-3. PMID 12650852.
• Lesch KP, Gutknecht L (2004). "Focus on The 5-HT1A receptor: emerging role of a gene regulatory variant in psychopathology and pharmacogenetics". Int. J. Neuropsychopharmacol. 7 (4): 381–5. doi:10.1017/S1461145704004845. PMID 15683551.
• Kalipatnapu S, Chattopadhyay A (2005). "Membrane protein solubilization: recent advances and challenges in solubilization of serotonin1A receptors". IUBMB Life. 57 (7): 505–12. doi:10.1080/15216540500167237. PMID 16081372.
• Varrault A, Bockaert J, Waeber C (1992). "Activation of 5-HT1A receptors expressed in NIH-3T3 cells induces focus formation and potentiates EGF effect on DNA synthesis". Mol. Biol. Cell. 3 (9): 961–9. doi:10.1091/mbc.3.9.961. PMC 275657. PMID 1330092.
• Levy FO, Gudermann T, Perez-Reyes E, Birnbaumer M, Kaumann AJ, Birnbaumer L (1992). "Molecular cloning of a human serotonin receptor (S12) with a pharmacological profile resembling that of the 5-HT1D subtype". J. Biol. Chem. 267 (11): 7553–62. PMID 1559993.
• Melmer G, Sherrington R, Mankoo B, Kalsi G, Curtis D, Gurling HM (1991). "A cosmid clone for the 5HT1A receptor (HTR1A) reveals a TaqI RFLP that shows tight linkage to dna loci D5S6, D5S39, and D5S76". Genomics. 11 (3): 767–9. doi:10.1016/0888-7543(91)90088-V. PMID 1685484.
• Parks CL, Chang LS, Shenk T (1991). "A polymerase chain reaction mediated by a single primer: cloning of genomic sequences adjacent to a serotonin receptor protein coding region". Nucleic Acids Res. 19 (25): 7155–60. doi:10.1093/nar/19.25.7155. PMC 332551. PMID 1766875.
• Gilliam TC, Freimer NB, Kaufmann CA, Powchik PP, Bassett AS, Bengtsson U, Wasmuth JJ (1989). "Deletion mapping of DNA markers to a region of chromosome 5 that cosegregates with schizophrenia". Genomics. 5 (4): 940–4. doi:10.1016/0888-7543(89)90138-9. PMC 3154173. PMID 2591972.
• Kobilka BK, Frielle T, Collins S, Yang-Feng T, Kobilka TS, Francke U, Lefkowitz RJ, Caron MG (1987). "An intronless gene encoding a potential member of the family of receptors coupled to guanine nucleotide regulatory proteins". Nature. 329 (6134): 75–9. Bibcode:1987Natur.329...75K. doi:10.1038/329075a0. PMID 3041227.
• Fargin A, Raymond JR, Lohse MJ, Kobilka BK, Caron MG, Lefkowitz RJ (1988). "The genomic clone G-21 which resembles a beta-adrenergic receptor sequence encodes the 5-HT1A receptor". Nature. 335 (6188): 358–60. doi:10.1038/335358a0. PMID 3138543.
• Nakhai B, Nielsen DA, Linnoila M, Goldman D (1995). "Two naturally occurring amino acid substitutions in the human 5-HT1A receptor: glycine 22 to serine 22 and isoleucine 28 to valine 28". Biochem. Biophys. Res. Commun. 210 (2): 530–6. doi:10.1006/bbrc.1995.1692. PMID 7755630.
• Aune TM, McGrath KM, Sarr T, Bombara MP, Kelley KA (1993). "Expression of 5HT1a receptors on activated human T cells. Regulation of cyclic AMP levels and T cell proliferation by 5-hydroxytryptamine". J. Immunol. 151 (3): 1175–83. PMID 8393041.
• Parks CL, Shenk T (1996). "The serotonin 1a receptor gene contains a TATA-less promoter that responds to MAZ and Sp1". J. Biol. Chem. 271 (8): 4417–30. doi:10.1074/jbc.271.8.4417. PMID 8626793.
• Stockmeier CA, Shapiro LA, Dilley GE, Kolli TN, Friedman L, Rajkowska G (1998). "Increase in serotonin-1A autoreceptors in the midbrain of suicide victims with major depression-postmortem evidence for decreased serotonin activity". J. Neurosci. 18 (18): 7394–401. doi:10.1523/JNEUROSCI.18-18-07394.1998. PMC 6793229. PMID 9736659.
• Kawanishi Y, Harada S, Tachikawa H, Okubo T, Shiraishi H (1998). "Novel mutations in the promoter and coding region of the human 5-HT1A receptor gene and association analysis in schizophrenia". Am. J. Med. Genet. 81 (5): 434–9. doi:10.1002/(SICI)1096-8628(19980907)81:5<434::AID-AJMG13>3.0.CO;2-D. PMID 9754630.
• Salim K, Fenton T, Bacha J, Urien-Rodriguez H, Bonnert T, Skynner HA, Watts E, Kerby J, Heald A, Beer M, McAllister G, Guest PC (2002). "Oligomerization of G-protein-coupled receptors shown by selective co-immunoprecipitation". J. Biol. Chem. 277 (18): 15482–5. doi:10.1074/jbc.M201539200. PMID 11854302.
• Panesar, Kiran. "5-HT1A Receptors in Psychopharmacology". Web Article. Psychopharmacology Institute. Retrieved 11 April 2013.

External links

• "5-HT_1A". IUPHAR Database of Receptors and Ion Channels. International Union of Basic and Clinical Pharmacology.
• Human HTR1A genome location and HTR1A gene details page in the UCSC Genome Browser.

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