HT1B receptor

HT1B receptor

5-hydroxytryptamine (serotonin) receptor 1B, G protein-coupled
Available structures
PDB Ortholog search: PDBe, RCSB
Identifiers
Symbols  ; 5-HT1B; 5-HT1DB; HTR1D2; HTR1DB; S12
External IDs IUPHAR: ChEMBL: GeneCards:
RNA expression pattern
Orthologs
Species Human Mouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)
RefSeq (protein)
Location (UCSC)
PubMed search

5-hydroxytryptamine receptor 1B also known as the 5-HT1B receptor is a protein that in humans is encoded by the HTR1B gene.[1][2] The 5-HT1B receptor is a 5-HT receptor subtype.[3]

Tissue distribution and function

5-HT1B receptors are widely distributed throughout the CNS with the highest concentrations found in the frontal cortex, basal ganglia, striatum, and the hippocampus.[4] The function of the 5-HT1B receptor differs depending upon its location. In the frontal cortex, it is believed to act as a postsynaptic receptor inhibiting the release of dopamine. In the basal ganglia and the striatum, evidence suggests 5-HT signaling acts on an autoreceptor, inducing the release of serotonin[5] and decreasing glutamatergic transmission by reducing miniature excitatory postsynaptic potential (mEPSP) frequency,[6] respectively. In the hippocampus, a recent study has demonstrated that activation of postsynaptic 5-HT1B heteroreceptors produces a facilitation in excitatory synaptic transmission which is altered in depression.[7] When the expression of 5-HT1B in human cortex is traced throughout life, A significant changes during adolescence was observed, in a way that is strongly correlated with the expression of 5-HT1E.[8]

Outside the brain, 5-HT1B receptor activation also has vascular effects, such as pulmonary vasoconstriction. Furthermore, blocking 5-HT1B receptor signaling decreases the number of osteoblasts, bone mass, and the bone formation rate.[9]

Knockout mice lacking the 5-HT1B gene have shown an increase in aggression and a higher preference for alcohol.[10] Under basal conditions, knockout mice present with a "normal" phenotype and an exhibit a sucrose preference (lack of sucrose preference is considered a measure of anhedonia). However, after undergoing chronic unpredictable stress treatment to induce a "depression-like" phenotype these animals do not benefit from administration of selective serotonin reuptake inhibitor (SSRIs).[7]

Ligands

Agonists

Partial agonists

Antagonists and inverse agonists

Genetics

In humans the protein is coded by the gene HTR1B.

A genetic variant in the promotor region, A-161T, has been examined with respect to personality traits and showed no major effect.[14]

See also

References

  1. ^ Jin H, Oksenberg D, Ashkenazi A, Peroutka SJ, Duncan AM, Rozmahel R, Yang Y, Mengod G, Palacios JM, O'Dowd BF (March 1992). "Characterization of the human 5-hydroxytryptamine1B receptor". J. Biol. Chem. 267 (9): 5735–8.  
  2. ^ Sanders AR, Cao Q, Taylor J, Levin TE, Badner JA, Cravchik A, Comeron JM, Naruya S, Del Rosario A, Salvi DA, Walczyk KA, Mowry BJ, Levinson DF, Crowe RR, Silverman JM, Gejman PV (February 2001). "Genetic diversity of the human serotonin receptor 1B (HTR1B) gene". Genomics 72 (1): 1–14.  
  3. ^ "Entrez Gene: HTR1B 5-hydroxytryptamine (serotonin) receptor 1B". 
  4. ^ "5-hydroxytryptamine (serotonin) receptor 1B, G protein-coupled". Retrieved 23 Feb 2013. 
  5. ^ Pytliak M, Vargová V, Mechírová V, Felšöci M (2011). "Serotonin receptors - from molecular biology to clinical applications". Physiol Res 60 (1): 15–25.  
  6. ^ Huang CC, Yeh CM, Wu MY, Hsu KS (2013). "A single in vivo cocaine administration impairs 5-HT1B receptor-induced long-term depression in the nucleus accumbens". J. Neurochem. 125 (6): 809–21.  
  7. ^ a b Cai X, Kallarackal AJ, Kvarta MD, Goluskin S, Gaylor K, Bailey AM, Lee HK, Huganir RL, Thompson SM (2013). "Local potentiation of excitatory synapses by serotonin and its alteration in rodent models of depression". Nat. Neurosci. 16 (4): 464–72.  
  8. ^ Shoval, G., Bar-Shira O., Zalsman G., John J. Mann and Chechik G. (2014) Transitions in the transcriptome of the serotonergic and dopaminergic systems in the human brain during adolescence. European Neuropsychopharmacology. (2014). "Transitions in the transcriptome of the serotonergic and dopaminergic systems in the human brain during adolescence". European neuropsychopharmacology 24 (7): 1123–32.  
  9. ^ Yadav VK, Ryu JH, Suda N, Tanaka KF, Gingrich JA, Schütz G, Glorieux FH, Chiang CY, Zajac JD, Insogna KL, Mann JJ, Hen R, Ducy P, Karsenty G (November 2008). "Lrp5 controls bone formation by inhibiting serotonin synthesis in the duodenum". Cell 135 (5): 825–37.  
  10. ^ Hoyer D, Hannon JP, Martin GR (2002). "Molecular, pharmacological and functional diversity of 5-HT receptors". Pharmacol. Biochem. Behav. 71 (4): 533–54.  
  11. ^ Hudzik, TJ; Yanek, M; Porrey, T; Evenden, J; Paronis, C; Mastrangelo, M; Ryan, C; Ross, S; Stenfors, C (2003). "Behavioral pharmacology of AR-A000002, a novel, selective 5-hydroxytryptamine(1B) antagonist.". The Journal of Pharmacology and Experimental Therapeutics 304 (3): 1072–84.  
  12. ^ Selkirk, JV; Scott, C; Ho, M; Burton, MJ; Watson, J; Gaster, LM; Collin, L; Jones, BJ; Middlemiss, DN; Price, GW (1998). "SB-224289--a novel selective (human) 5-HT1B receptor antagonist with negative intrinsic activity.". British Journal of Pharmacology 125 (1): 202–8.  
  13. ^ Roberts, C; Watson, J; Price, GW; Middlemiss, DN (2001). "SB-236057-A: a selective 5-HT1B receptor inverse agonist.". CNS Drug Reviews 7 (4): 433–44.  
  14. ^ Tsai SJ, Wang YC, Chen JY, Hong CJ (2003). "Allelic variants of the tryptophan hydroxylase (A218C) and serotonin 1B receptor (A-161T) and personality traits". Neuropsychobiology 48 (2): 68–71.  

External links

  • "1B"5-HT. IUPHAR Database of Receptors and Ion Channels. International Union of Basic and Clinical Pharmacology. 

Further reading

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