5-HT1A receptor

From Self-sufficiency
Jump to: navigation, search
5-hydroxytryptamine (serotonin) receptor 1A
SymbolsHTR1A; 5-HT1A; 5HT1a; ADRB2RL1; ADRBRL1
External IDsOMIM109760 MGI96273 HomoloGene20148 IUPHAR: 5-HT1A GeneCards: HTR1A Gene
RNA expression pattern
More reference expression data
RefSeq (mRNA)NM_000524NM_008308
RefSeq (protein)NP_000515NP_032334
Location (UCSC)Chr 5:
63.29 - 63.29 Mb
Chr 13:
106.56 - 106.57 Mb
PubMed search[1][2]

The 5-HT1A receptor is a subtype of 5-HT receptor that binds the endogenous neurotransmitter serotonin (5-hydroxytryptamine, 5-HT). It is a G protein-coupled receptor (GPCR) that is coupled to Gi/Go and mediates inhibitory neurotransmission. HTR1A denotes the human gene encoding for the receptor.[1][2]


The 5-HT1A receptor is the most widespread of all the 5-HT receptors. In the central nervous system, 5-HT1A receptors exist in the cerebral cortex, hippocampus, septum, amygdala, and raphe nucelus in high densities, while low amounts also exist in the basal ganglia and thalamus.[3][4][5] The 5-HT1A receptors in the raphe nucleus are largely somatodendritic autoreceptors, whereas those in other areas such as the hippocampus are postsynaptic receptors.[4]



5-HT1A receptor agonists decrease blood pressure and heart rate via a central mechanism, by inducing peripheral vasodilation, and by stimulating the vagus nerve.[6] These effects are the result of activation of 5-HT1A receptors within the rostral ventrolateral medulla.[6] The sympatholytic antihypertensive drug urapidil is an α1-adrenergic receptor antagonist and α2-adrenergic receptor agonist, as well as 5-HT1A receptor agonist, and it has been demonstrated that the latter property contributes to its overall therapeutic effects.[7][8] Vasodilation of the blood vessels in the skin via central 5-HT1A activation increases heat dissipation from the organism out into the environment, causing a decrease in body temperature.[9][10]

Activation of central 5-HT1A 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.[11][12][13]

5-HT1A receptor agonists like buspirone[14] and flesinoxan[15] show efficacy in relieving anxiety[16] and depression,[17] and buspirone and tandospirone are currently approved for these indications in various parts of the world. Others such as gepirone,[18] flesinoxan,[15] flibanserin,[19] and PRX-00023[20] have also been investigated, though none have been fully developed and approved as of yet. Some of the atypical antipsychotics like aripiprazole[21] are also partial agonists at the 5-HT1A receptor and are sometimes used in low doses as augmentations to standard antidepressants like the selective serotonin reuptake inhibitors (SSRIs).[22]

5-HT1A autoreceptor desensitization and increased 5-HT1A 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).[23] 5-HT1A receptor activation likely plays a significant role in the positive effects of serotonin releasing agents (SRAs) like MDMA ("Ecstasy") as well.[24][25]

5-HT1A 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.[26][27] In addition to being antidepressant and anxiolytic in effect, 5-HT1A receptor activation has also been demonstrated to be antiemetic[28][29] and analgesic,[30][31] 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.[32]

5-HT1A 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.[33][34] As mentioned above, some of the atypical antipsychotics are 5-HT1A receptor partial agonists, and this property has been shown to enhance their clinical efficacy.[33][35][36] 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-HT1A receptor.[37][38]

Activation of 5-HT1A receptors has been demonstrated to impair cognition, learning, and memory by inhibiting the release of glutamate and acetylcholine in various areas of the brain.[39] Conversely, 5-HT1A 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.[40]

Other effects of 5-HT1A activation include decreased aggression or increased serenic behavior,[41][42] increased sociability,[25] increased impulsivity,[43] inhibition of addictive behavior,[44][45][46] facilitation of sexual behavior and arousal,[47][48] inhibition of penile erection,[49][50] decreased food intake or anorexia,[51] prolongation of REM sleep latency,[52][53] and enhanced breathing or hyperventilation and reversal of opioid-induced respiratory depression.[54]


5-HT1A receptor activation induces the secretion of various hormones including cortisol, corticosterone, adrenocorticotropic hormone (ACTH), oxytocin, prolactin, growth hormone, and β-endorphin.[55][56][57][58] The receptor does not affect vasopressin or renin secretion, unlike the 5-HT2 receptors.[55][56] It has been suggested that oxytocin release may contribute to the prosocial, antiaggressive or serenic, and anxiolytic properties observed upon activation of the receptor.[25] β-Endorphin secretion likely contributes to antidepressant, anxiolytic, and analgesic effects.


5-HT1A receptors can be located on the cell body or soma, dendrites, axons, and both presynaptically and postsynaptically in nerve terminals or synapses. Those located on the soma and dendrites are called somatodendritic, and those located presynaptically in the synapse are aptly titled presynaptic. As a group, they are known as autoreceptors. Stimulation of 5-HT1A autoreceptors inhibits the release of serotonin in nerve terminals. For this reason, 5-HT1A receptor agonists tend to exert a biphasic mode of action; they decrease serotonin release and postsynaptic 5-HT1A receptor activity in low doses, and further decrease serotonin release but increase postsynaptic 5-HT1A receptor activity at moderate to high doses by directly stimulating the receptors in replacement of serotonin.

This autoreceptor-mediated inhibition of serotonin release has been postulated to be one of the reasons for the therapeutic lag that is commonly reported for most mainstream serotonergic antidepressants such as the SSRIs.[59] The autoreceptors must first densensitize before the concentration of extracellular serotonin in the synapse can become elevated appreciably.[59][60] Though the responsiveness of the autoreceptors is somewhat reduced with chronic treatment, they still remain effective at constraining large increases in extracellular serotonin concentrations.[59] For this reason, serotonin reuptake inhibitors that also have 5-HT1A receptor antagonistic or partial agonistic properties such as vilazodone and SB-649,915 are currently being investigated as novel antidepressants with a faster onset of action and greater efficacy than many of those currently available.[61]

Unlike most drugs that elevate extracellular serotonin levels like the SSRIs and MAOIs, SRAs such as fenfluramine and MDMA ("Ecstasy") fully bypass serotonin autoreceptors like 5-HT1A by forcing release to occur regardless of their inhibition.[62] This is why SRAs display immediate and full effects in contrast to drugs like the SSRIs, which require several weeks of chronic dosing before therapeutic benefits are seen, and also why SRAs are much stronger than SSRIs and related compounds in effect as they produce far more robust and balanced increases in extracellular serotonin concentrations.[63][64] For these reasons, selective serotonin releasing agents (SSRAs) including MDAI, MMAI, and 4-MTA have been proposed as novel antidepressants with an immediate onset of action and far greater efficacy in comparison to most current treatments.[63]

Sufficient doses of 5-HT1A receptor agonists themselves, like SRAs, are capable of fully bypassing the 5-HT1A autoreceptor-mediated inhibition of serotonin release and therefore decreased 5-HT1A postsynaptic receptor activation as well, by directly agonizing the postsynaptic receptors in lieu of serotonin. It is mentionable, however, that, unlike SRAs, 5-HT1A receptor agonists are incapable of bypassing the inhibitory effect of 5-HT1A autoreceptors located as heteroreceptors in non-serotonergic synapses where 5-HT1A postsynaptic receptors are not present, which, instead of serotonin, modulate the release of other neurotransmitters such as dopamine or glutamate.


The distribution of 5-HT1A receptors in the human brain may be imaged with the positron emission tomography using the radioligand [11C]WAY-100,635.[65] For example, one study has found increased 5-HT1A binding in type 2 diabetes.[66] Another PET study found a negative correlation between the amount of 5-HT1A binding in the raphe nuclei, hippocampus and neocortex and a self-reported tendency to have spiritual experiences.[67] Labeled with tritium, WAY-100,635 may also be used in autoradiography.[68]




The 5-HT1A 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).[69] The most investigated SNPs are C-1019G (rs6295), C-1018G,[70] Ile28Val (rs1799921), Arg219Leu (rs1800044), and Gly22Ser (rs1799920).[69] 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.[69]


The 5-HT1A 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.[71][72] It has also been shown to interact with sphingosine-1-phosphate receptor 1 (S1PR1).[73]

See also


Cite error: Invalid <references> tag; parameter "group" is allowed only.

Use <references />, or <references group="..." />

Further reading

  • el Mestikawy S, Fargin A, Raymond JR; et al. (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 (2005). "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 (2006). "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. PMC 275657Freely accessible. PMID 1330092. 
  • Levy FO, Gudermann T, Perez-Reyes E; et al. (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; et al. (1992). "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 (1992). "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 332551Freely accessible. PMID 1766875. 
  • Gilliam TC, Freimer NB, Kaufmann CA; et al. (1990). "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. PMID 2591972. 
  • Kobilka BK, Frielle T, Collins S; et al. (1987). "An intronless gene encoding a potential member of the family of receptors coupled to guanine nucleotide regulatory proteins". Nature. 329 (6134): 75–9. doi:10.1038/329075a0. PMID 3041227. 
  • Fargin A, Raymond JR, Lohse MJ; et al. (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; et al. (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; et al. (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. PMID 9736659. 
  • Kawanishi Y, Harada S, Tachikawa H; et al. (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; et al. (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. 

External links

  • "5-HT1A". IUPHAR Database of Receptors and Ion Channels. International Union of Basic and Clinical Pharmacology. 

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

  1. Lua error in package.lua at line 80: module 'Module:Citation/CS1/Suggestions' not found.
  2. "Entrez Gene: HTR1A 5-hydroxytryptamine (serotonin) receptor 1A". 
  3. Ito H, Halldin C, Farde L. (1999). "Localization of 5-HT1A receptors in the living human brain using [carbonyl-11C]WAY-100635: PET with anatomic standardization technique". J Nucl Med. 40 (1): 102–109. PMID 9935065. 
  4. 4.0 4.1 Glennon RA, Dukat M, Westkaemper RB (2000-01-01). "Serotonin Receptor Subtypes and Ligands". American College of Neurophyscopharmacology. Retrieved 2008-04-11. 
  5. de Almeida J, Mengod G. (2008). "Serotonin 1A receptors in human and monkey prefrontal cortex are mainly expressed in pyramidal neurons and in a GABAergic interneuron subpopulation: implications for schizophrenia and its treatment". J Neurochem. 107 (2): 488–496. doi:10.1111/j.1471-4159.2008.05649.x. PMID 18761712. 
  6. 6.0 6.1 Dabiré H. (1991). "Central 5-hydroxytryptamine (5-HT) receptors in blood pressure regulation". Therapie. 46 (6): 421–9. PMID 1819150. 
  7. Lua error in package.lua at line 80: module 'Module:Citation/CS1/Suggestions' not found.
  8. Kolassa N, Beller KD, Sanders KH. (1989). "Involvement of brain 5-HT1A receptors in the hypotensive response to urapidil". Am J Cardiol. 64 (7): 7D–10D. doi:10.1016/0002-9149(89)90688-7. PMID 2569265. 
  9. Ootsuka Y, Blessing WW. (2006). "Activation of 5-HT1A receptors in rostral medullary raphé inhibits cutaneous vasoconstriction elicited by cold exposure in rabbits". Brain Res. 1073-1074: 252–61. doi:10.1016/j.brainres.2005.12.031. PMID 16455061. 
  10. Rusyniak DE, Zaretskaia MV, Zaretsky DV, DiMicco JA. (2007). "3,4-Methylenedioxymethamphetamine- and 8-hydroxy-2-di-n-propylamino-tetralin-induced hypothermia: role and location of 5-hydroxytryptamine 1A receptors". J Pharmacol Exp Ther. 323 (2): 477–487. doi:10.1124/jpet.107.126169. PMID 17702902. 
  11. Yu Y, Ramage AG, Koss MC. (2004). "Pharmacological studies of 8-OH-DPAT-induced pupillary dilation in anesthetized rats". Eur J Pharmacol. 489 (3): 207–213. doi:10.1016/j.ejphar.2004.03.007. PMID 15087245. 
  12. Prow MR, Martin KF, Heal DJ (1996). "8-OH-DPAT-induced mydriasis in mice: a pharmacological characterisation". Eur J Pharmacol. 317 (1): 21–8. doi:10.1016/S0014-2999(96)00693-0. PMID 8982715. 
  13. Lua error in package.lua at line 80: module 'Module:Citation/CS1/Suggestions' not found.
  14. Lua error in package.lua at line 80: module 'Module:Citation/CS1/Suggestions' not found.
  15. 15.0 15.1 Cryan JF, Redmond AM, Kelly JP, Leonard BE. (1997). "The effects of the 5-HT1A agonist flesinoxan, in three paradigms for assessing antidepressant potential in the rat". Eur Neuropsychopharmacol. 7 (2): 109–114. doi:10.1016/S0924-977X(96)00391-4. PMID 9169298. 
  16. Parks CL, Robinson PS, Sibille E, Shenk T, Toth M (1998). "Increased anxiety of mice lacking the serotonin1A receptor". Proc Natl Acad Sci U S A. 195 (18): 10734–9. doi:10.1073/pnas.95.18.10734. PMC 27964Freely accessible. PMID 9724773. 
  17. Kennett GA, Dourish CT, Curzon G (1987). "Antidepressant-like action of 5-HT1A agonists and conventional antidepressants in an animal model of depression". Eur J Pharmacol. 134 (3): 265–74. doi:10.1016/0014-2999(87)90357-8. PMID 2883013. 
  18. Lua error in package.lua at line 80: module 'Module:Citation/CS1/Suggestions' not found.
  19. Lua error in package.lua at line 80: module 'Module:Citation/CS1/Suggestions' not found.
  20. de Paulis T. (2007). "Drug evaluation: PRX-00023, a selective 5-HT1A receptor agonist for depression". Curr Opin Investig Drugs. 8 (1): 78–86. PMID 17263189. 
  21. Stark, AD; et al. (2007). "Interaction of the novel antipsychotic aripiprazole with 5-HT1A and 5-HT2A receptors: functional receptor-binding and in vivo electrophysiological studies". Psychopharmacology (Berl). 190 (3): 373–382. doi:10.1007/s00213-006-0621-y. PMID 17242925. 
  22. Lua error in package.lua at line 80: module 'Module:Citation/CS1/Suggestions' not found.
  23. Lua error in package.lua at line 80: module 'Module:Citation/CS1/Suggestions' not found.
  24. Lua error in package.lua at line 80: module 'Module:Citation/CS1/Suggestions' not found.
  25. 25.0 25.1 25.2 Lua error in package.lua at line 80: module 'Module:Citation/CS1/Suggestions' not found.
  26. Lua error in package.lua at line 80: module 'Module:Citation/CS1/Suggestions' not found.
  27. Baker KG, Halliday GM, Hornung J-P, Geffen LB, Cotton RGH, Tork I. Distribution, morphology and number of monoamine-synthesizing and substance P-containing neurons in the human dorsal raphe nucleus. Neuroscience. 1991;42(3):757-75.
  28. Lua error in package.lua at line 80: module 'Module:Citation/CS1/Suggestions' not found.
  29. Lua error in package.lua at line 80: module 'Module:Citation/CS1/Suggestions' not found.
  30. Lua error in package.lua at line 80: module 'Module:Citation/CS1/Suggestions' not found.
  31. Lua error in package.lua at line 80: module 'Module:Citation/CS1/Suggestions' not found.
  32. Blier P, Gobbi G, Haddjeri N, Santarelli L, Mathew G, Hen R. (2004). "Impact of substance P receptor antagonism on the serotonin and norepinephrine systems: relevance to the antidepressant/anxiolytic response". J Psychiatry Neurosci. 29 (3): 208–218. PMC 400690Freely accessible. PMID 15173897. 
  33. 33.0 33.1 Li Z, Ichikawa J, Dai J, Meltzer HY. (2004). "Aripiprazole, a novel antipsychotic drug, preferentially increases dopamine release in the prefrontal cortex and hippocampus in rat brain". Eur J Pharmacol. 498 (1-3): 75–83. doi:10.1016/j.ejphar.2004.04.028. PMID 15189766. 
  34. Bantick RA, De Vries MH, Grasby PM. (2005). "The effect of a 5-HT1A receptor agonist on striatal dopamine release". Synapse. 57 (2): 67–75. doi:10.1002/syn.20156. PMID 15906386. 
  35. Rollema H, Lu Y, Schmidt AW, Sprouse JS, Zorn SH. (2000). "5-HT(1A) receptor activation contributes to ziprasidone-induced dopamine release in the rat prefrontal cortex". Biol Psychiatry. 48 (3): 229–237. doi:10.1016/S0006-3223(00)00850-7. PMID 10924666. 
  36. Rollema H, Lu Y, Schmidt AW, Zorn SH. (1997). "Clozapine increases dopamine release in prefrontal cortex by 5-HT1A receptor activation". Eur J Pharmacol. 338 (2): R3–5. doi:10.1016/S0014-2999(97)81951-6. PMID 9456005. 
  37. Lua error in package.lua at line 80: module 'Module:Citation/CS1/Suggestions' not found.
  38. Lua error in package.lua at line 80: module 'Module:Citation/CS1/Suggestions' not found.
  39. Ogren SO, Eriksson TM, Elvander-Tottie E, D'Addario C, Ekström JC, Svenningsson P, Meister B, Kehr J, Stiedl O (2008). "The role of 5-HT(1A) receptors in learning and memory". Behav Brain Res. 195 (1): 54–77. doi:10.1016/j.bbr.2008.02.023. PMID 18394726. 
  40. H. Spreitzer (August 13, 2008). "Neue Wirkstoffe - Lecozotan". Österreichische Apothekerzeitung (in German) (17/2007): 805. 
  41. de Boer SF, Koolhaas JM (2005). "5-HT1A and 5-HT1B receptor agonists and aggression: a pharmacological challenge of the serotonin deficiency hypothesis". Eur J Pharmacol. 526 (1-3): 125–39. doi:10.1016/j.ejphar.2005.09.065. PMID 18853336. 
  42. Olivier B, Mos J, Rasmussen D. (1990). "Behavioural pharmacology of the serenic, eltoprazine". Drug Metabol Drug Interact. 8 (1-2): 31–83. PMID 2091890. 
  43. Winstanley CA, Theobald DE, Dalley JW, Robbins TW. (2005). "Interactions between serotonin and dopamine in the control of impulsive choice in rats: therapeutic implications for impulse control disorders". Neuropsychopharmacology. 30 (4): 669–682. doi:10.1038/sj.npp.1300610. PMID 15688093. 
  44. Tomkins DM, Higgins GA, Sellers EM (1994). "Low doses of the 5-HT1A agonist 8-hydroxy-2-(di-n-propylamino)-tetralin (8-OH DPAT) increase ethanol intake". Psychopharmacology (Berl). 115 (1-2): 173–9. doi:10.1007/BF02244769. PMID 7862892. 
  45. Müller CP, Carey RJ, Huston JP, De Souza Silva MA (2007). "Serotonin and psychostimulant addiction: focus on 5-HT1A-receptors". Prog Neurobiol. 81 (3): 133–78. doi:10.1016/j.pneurobio.2007.01.001. PMID 17316955. 
  46. Carey RJ, DePalma G, Damianopoulos E, Shanahan A, Müller CP, Huston JP (2005). "Evidence that the 5-HT1A autoreceptor is an important pharmacological target for the modulation of cocaine behavioral stimulant effects". Brain Res. 1034 (1-2): 162–71. doi:10.1016/j.brainres.2004.12.012. PMID 15713268. 
  47. Lua error in package.lua at line 80: module 'Module:Citation/CS1/Suggestions' not found.
  48. Lua error in package.lua at line 80: module 'Module:Citation/CS1/Suggestions' not found.
  49. Simon P, Guardiola B, Bizot-Espiard J, Schiavi P, Costentin J (1992). "5-HT1A receptor agonists prevent in rats the yawning and penile erections induced by direct dopamine agonists". Psychopharmacology. 108 (1-2): 47–50. doi:10.1007/BF02245284. PMID 1357709. 
  50. Millan MJ, Perrin-Monneyron S (1997). "Potentiation of fluoxetine-induced penile erections by combined blockade of 5-HT1A and 5-HT1B receptors". Eur J Pharmacol. 321 (3): 11–3. doi:10.1016/S0014-2999(97)00050-2. PMID 9085055. 
  51. Ebenezer IS, Arkle MJ, Tite RM (1998). "8-Hydroxy-2-(di-n-propylamino)-tetralin inhibits food intake in fasted rats by an action at 5-HT1A receptors". Methods Find Exp Clin Pharmacol. 29 (4): 269–72. doi:10.1358/mf.2007.29.4.1075362. PMID 17609739. 
  52. Monti JM, Jantos H (1992). "Dose-dependent effects of the 5-HT1A receptor agonist 8-OH-DPAT on sleep and wakefulness in the rat". J Sleep Res. 1 (3): 169–175. doi:10.1111/j.1365-2869.1992.tb00033.x. PMID 10607047. 
  53. Marc Ansseau, William Pitchot, Antonio Gonzalez Moreno, Jacques Wauthy, Patrick Papart (2004). "Pilot study of flesinoxan, a 5-HT1A agonist, in major depression: Effects on sleep REM latency and body temperature". Human Psychopharmacology: Clinical and Experimental. 8 (4): 279–283. doi:10.1002/hup.470080407. 
  54. Lua error in package.lua at line 80: module 'Module:Citation/CS1/Suggestions' not found.
  55. 55.0 55.1 Van de Kar LD, Levy AD, Li Q, Brownfield MS. (1998). "A comparison of the oxytocin and vasopressin responses to the 5-HT1A agonist and potential anxiolytic drug alnespirone (S-20499)". Pharmacol Biochem Behav. 60 (3): 677–683. doi:10.1016/S0091-3057(98)00025-2. PMID 9678651. 
  56. 56.0 56.1 Lorens SA, Van de Kar LD. (1987). "Differential effects of serotonin (5-HT1A and 5-HT2) agonists and antagonists on renin and corticosterone secretion". Neuroendocrinology. 45 (4): 305–310. doi:10.1159/000124754. PMID 2952898. 
  57. Koenig JI, Gudelsky GA, Meltzer HY. (1987). "Stimulation of corticosterone and beta-endorphin secretion in the rat by selective 5-HT receptor subtype activation". Eur J Pharmacol. 137 (1): 1–8. doi:10.1016/0014-2999(87)90175-0. PMID 2956114. 
  58. Lua error in package.lua at line 80: module 'Module:Citation/CS1/Suggestions' not found.
  59. 59.0 59.1 59.2 Hjorth S, Bengtsson HJ, Kullberg A, Carlzon D, Peilot H, Auerbach SB. (2000). "Serotonin autoreceptor function and antidepressant drug action". J Psychopharmacol. 14 (2): 177–185. doi:10.1177/026988110001400208. PMID 10890313. 
  60. Briley M, Moret C. (1993). "Neurobiological mechanisms involved in antidepressant therapies". Clin Neuropharmacol. 16 (5): 387–400. doi:10.1097/00002826-199310000-00002. PMID 8221701. 
  61. Starr KR, Price GW, Watson JM, Atkinson PJ, Arban R, Melotto S, Dawson LA, Hagan JJ, Upton N, Duxon MS. (2007). "SB-649915-B, a novel 5-HT1A/B autoreceptor antagonist and serotonin reuptake inhibitor, is anxiolytic and displays fast onset activity in the rat high light social interaction test". Neuropsychopharmacology. 32 (10): 2163–2172. doi:10.1038/sj.npp.1301341. PMID 17356576. 
  62. Rothman RB, Baumann MH (2006). "Therapeutic potential of monoamine transporter substrates". Current Topics in Medicinal Chemistry. 6 (17): 1845–59. doi:10.2174/156802606778249766. PMID 17017961. 
  63. 63.0 63.1 Lua error in package.lua at line 80: module 'Module:Citation/CS1/Suggestions' not found.
  64. Lua error in package.lua at line 80: module 'Module:Citation/CS1/Suggestions' not found.
  65. Pike VW, McCarron JA, Lammerstma AA, Hume SP, Poole K, Grasby PM, Malizia A, Cliffe IA, Fletcher A, Bench CJ (1995). "First delineation of 5-HT1A receptors in human brain with PET and [11C]WAY-100635". Eur. J. Pharmacol. 283 (1-3): R1–3. doi:10.1016/0014-2999(95)00438-Q. PMID 7498295. 
  66. Price JC, Kelley DE, Ryan CM, Meltzer CC, Drevets WC, Mathis CA, Mazumdar S, Reynolds CF (2002). "Evidence of increased serotonin-1A receptor binding in type 2 diabetes: a positron emission tomography study". Brain Res. 927 (1): 97–103. doi:10.1016/S0006-8993(01)03297-8. PMID 11814436. 
  67. Lua error in package.lua at line 80: module 'Module:Citation/CS1/Suggestions' not found.
  68. Burnet PW, Eastwood SL, Harrison PJ (1997). "[3H]WAY-100635 for 5-HT1A receptor autoradiography in human brain: a comparison with [3H]8-OH-DPAT and demonstration of increased binding in the frontal cortex in schizophrenia". Neurochem. Int. 30 (6): 565–574. doi:10.1016/S0197-0186(96)00124-6. PMID 9152998. 
  69. 69.0 69.1 69.2 Lua error in package.lua at line 80: module 'Module:Citation/CS1/Suggestions' not found.
  70. Lua error in package.lua at line 80: module 'Module:Citation/CS1/Suggestions' not found.
  71. Anttila S, Huuhka K, Huuhka M, Rontu R, Hurme M, Leinonen E; et al. (2007). "Interaction between 5-HT1A and BDNF genotypes increases the risk of treatment-resistant depression". J Neural Transm. 114 (8): 1065–8. doi:10.1007/s00702-007-0705-9. PMID 17401528. 
  72. Guiard BP, David DJ, Deltheil T, Chenu F, Le Maître E, Renoir T; et al. (2008). "Brain-derived neurotrophic factor-deficient mice exhibit a hippocampal hyperserotonergic phenotype". Int J Neuropsychopharmacol. 11 (1): 79–92. doi:10.1017/S1461145707007857. PMID 17559709. 
  73. Lua error in package.lua at line 80: module 'Module:Citation/CS1/Suggestions' not found.