Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P08908 (5-HT1A)
 5,574 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serotonin (5-hydroxytryptamine; 5-HT) modulates constituents of the immune system. 5-HT1A receptor antagonists potently suppress lymphocyte function. NK cell activity (NKCA) was measured after exposure of mononuclear cells to the 5-HT1A receptor antagonist pindobind and the 5-HT(1C/2) receptor antagonist ketanserin. Elutriated monocytes were exposed to pindobind, incubated with peripheral blood lymphocytes (PBL) in the presence or absence of an H2O2 scavenger catalase, and NKCA measured. Pindobind, but not ketanserin, suppressed NKCA in vitro. Pindobind-treated monocytes suppressed NKCA, whereas pindobind treatment of PBL did not affect NKCA. Catalase inhibited pindobind-induced suppression of NKCA. These data are consistent with previous results that 5-HT modulates NKCA via 5-HT1A receptors on monocytes and suggest that 5-HT may abrogate monocyte suppression of NKCA by inhibiting monocyte signals such as H2O2.
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PMID:Monocyte 5-HT1A receptors mediate pindobind suppression of natural killer cell activity: modulation by catalase. 1136 Sep 26

Mice exposed to various stresses, especially restrained-stress, revealed the anxiogenic effect detected by the light-dark test. Under this condition, a remarkable decrease in [35S]GTPgammaS binding to membranes from the prefrontal cortex, amygdala and hypothalamus of restrained-stress mice stimulated by the selective 5-HT1A receptor agonist 5-carboxamidotriptamine (5-CT) was clearly observed, whereas a significant increase in [35S]GTPgammaS binding stimulated by the 5-HT1A receptor agonist was clearly observed in the dorsal raphe nuclei (DRN) of restrained-stress mice. The immunohistochemical study showed a drastic reduction in phosphorylated-CREB-like immunoreactivity in the DRN of restrained-stress mice. Furthermore, we found a drastic reduction in myelin-associated glycoprotein (MAG)-like immunoreactivity (MAG-IR) in the DRN, amygdala and hypothalamus, indicating the direct suppression of synaptic transmission in these regions. It has been accepted that GSK3beta in the Wnt signal pathway plays an important role in various neuronal functions including apoptosis, clustering of synapsin I and early growth and axonal remodeling. In the present study, the increase in protein levels of GSK3beta and phosphorylated-GSK3beta to cytosol fractions of the amygdala was noted in restrained-stress mice. Taken together, these results suggest that restrained stress may directly affect the 5-HT1A receptor-regulated synaptic transmission in the brain, leading to the expression of the anxiogenic effect in mice. It is well known that various stresses induce intracellular oxidative stress. The present study was then undertaken to investigate the effect of the stimulation of 5-HT1A receptors on oxidative stress. Treatment with H2O2 caused the activation of caspase-3-positive cells and the reduction in levels of MAG-IR in the limbic neuron/glia cocultures as compared to medium alone. The stimulation of 5-HT1A receptor by 5-CT produced a dramatic protection against H2O2-triggered activation of caspase-3 and reduction in levels of MAG-IR. These results suggest that 5-HT1A receptors were involved in the modulation of anxiety and the understanding of molecular mechanisms of 5-HT1A receptor-related cascades may pave the way for new therapeutic strategies for affective disorders.
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PMID:[The functional change in the 5-HT1A receptor induced by stress and the role of the 5-HT1A receptor in neuroprotection]. 1622 Jun 59