Serotonin 5-HT1A receptor and Serotonin 5-HT1B receptor (5-HT1A and 5-HT1B receptor)

The **serotonin 5-HT1A receptor** and **5-HT1B receptor** are both class A G protein-coupled receptors (GPCRs) and key components of the serotonin (5-hydroxytryptamine, 5-HT) signaling system. They are widely distributed in the central nervous system and peripheral tissues, with high expression in brain regions involved in emotion, cognition, and vascular control. The 5-HT1A receptor mediates serotonergic signal transduction primarily via Gi/o protein coupling, leading to inhibition of neuronal firing, modulation of neurotransmitter release, and regulation of hormonal secretion; presynaptically, it acts as an autoreceptor in the raphe nuclei, and postsynaptically, it modulates regions like the hippocampus and cortex[1][3][4][6]. The 5-HT1B receptor is also a Gi/o-coupled GPCR extensively expressed on presynaptic axon terminals of serotonergic and non-serotonergic neurons, where it inhibits release of serotonin and other neurotransmitters; it is particularly involved in regulating mood, addiction, migraine, and vascular tone[2][5]. Both receptors are critical therapeutic targets for neuropsychiatric conditions (such as anxiety, depression, and OCD) and for migraine, with drugs targeting them as agonists or antagonists to modulate serotonergic transmission. Due to their involvement in vital CNS and peripheral functions, their pharmacological modulation must be carefully managed to avoid psychiatric or cardiovascular adverse effects.

Other names

5-hydroxytryptamine receptor 1A (5-HT1A)5-hydroxytryptamine receptor 1B (5-HT1B)HTR1A (gene symbol for 5-HT1A)HTR1B (gene symbol for 5-HT1B)Serotonin receptor 1ASerotonin receptor 1B5-HT1A autoreceptor5-HT1B autoreceptor

Agonists activate Gi/o-coupled signaling pathways reducing cAMP levels, leading to neuronal hyperpolarization and reduced neurotransmitter release Inhibition of neurotransmitter (including serotonin, GABA, glutamate, noradrenaline, acetylcholine) release via presynaptic autoreceptor and heteroreceptor action (especially 5-HT1B) Vasoconstriction of cranial blood vessels (migraine therapy, 5-HT1B) Modulation of neuroendocrine hormone release (5-HT1A) Inverse agonists/antagonists block basal or ligand-induced receptor activity, increasing serotonin levels at synapses