Английская Википедия:5-HT1B receptor

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Шаблон:Short description

Шаблон:Infobox gene 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 central nervous system 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 terminal receptor inhibiting the release of dopamine. In the basal ganglia and the striatum, evidence suggests 5-HT signaling acts on an autoreceptor, inhibiting 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 was traced throughout life, significant changes during adolescence were observed, in a way that is strongly correlated with the expression of 5-HT1E.[8]

Outside of the CNS, the 5-HT1B receptor is also expressed on the endothelium of blood vessels, particularly in the meninges.[9] Activation of these receptors results in vasoconstriction. The high distribution of vasoconstrictive 5-HT1B and 5-HT1D receptors around the brain makes them a valuable drug target for the treatment of migraines.[9]

Blocking 5-HT1B receptor signalling also increases the number of osteoblasts, bone mass, and the bone formation rate.[10]

Knockout mice lacking the 5-HT1B gene have been reported to have a higher preference for alcohol, although later studies failed to replicate such abnormalities in alcohol consumption.[11] These mice have also been reported to have a lower measure of anxiety (such as on the elevated plus maze test) and a higher measure of aggression.[11]

Under basal conditions, knockout mice present with a "normal" phenotype and 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]Шаблон:Failed verification

Ligands

Agonists

Partial agonists

Antagonists and inverse agonists

Undetermined Action

Genetics

In humans the protein is coded by the gene HTR1B.

A genetic variant in the promoter region, A-161T, has been examined with respect to personality traits and showed no major effect.[16]

See also

References

Шаблон:Reflist

Further reading

Шаблон:Refbegin

Шаблон:Refend

External links

Шаблон:NLM content Шаблон:G protein-coupled receptors Шаблон:Serotonergics

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  1. ↑ Шаблон:Cite journal
  2. ↑ Шаблон:Cite journal
  3. ↑ Шаблон:Cite web
  4. ↑ Шаблон:Cite web
  5. ↑ Шаблон:Cite journal
  6. ↑ Шаблон:Cite journal
  7. ↑ 7,0 7,1 Шаблон:Cite journal
  8. ↑ Шаблон:Cite journal
  9. ↑ 9,0 9,1 Шаблон:Cite journal
  10. ↑ Шаблон:Cite journal
  11. ↑ 11,0 11,1 Шаблон:Cite journal
  12. ↑ Шаблон:Cite journal
  13. ↑ Шаблон:Cite journal
  14. ↑ Шаблон:Cite journal
  15. ↑ Шаблон:Cite journal
  16. ↑ Шаблон:Cite journal
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