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

We have previously reported that Quercetin 3-O-b-D-apiofuranosyl-(1-->2)-[a-L-rhamnopyranosyl-(1-->6)]-b-D-glucopyranoside (CTN-986), a potential antidepressant extracted from glandless cottonseeds, exerted a notable antidepressant-like effect in experimental animal models. Recent evidence suggested, at least in some animal models, that the behavioral effects of chronic antidepressant treatment were mediated by the stimulation of hippocampal neurogenesis. To explore possible mechanisms of CTN-986's antidepressant-like effect, CTN-986 (10 mg/kg, i.g) or imipramine (IMI, 10 mg/kg, i.g) was administered once per day to the chronically stressed mice over 21 days. Immunohistochemical analysis revealed that chronic CTN-986 treatment increased bromodeoxyuridine (BrdU; thymidine analog as a marker for dividing cells)-positive cells in the hippocampal dentate gyrus in stressed mice, as was the case with chronic IMI treatment. Moreover, using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT) assay and [3H] thymidine incorporation assay, it was found that exposure to CTN-986 for 4 days dose-dependently increased the proliferation of the cultured hippocampal neural progenitor cells (NPCs). This effect was significantly reversed by co-incubation with serotonin 1A (5-HT1A) receptor antagonist WAY100635. These results indicate that CTN-986 increase hippocampal NPCs proliferation which might be closely related to the activation of the 5-HT1A receptor. This finding can shed light on the mechanisms for its antidepressant-like effects.
 ...
PMID:CTN-986, a compound extracted from cottonseeds, increases cell proliferation in hippocampus in vivo and in cultured neural progenitor cells in vitro. 1932 68

Previous preclinical studies have demonstrated that cannabidiol (CBD) and cannabigerol (CBG), two non-psychotomimetic phytocannabinoids from Cannabis sativa, induce neuroprotective effects on toxic and neurodegenerative processes. However, a comparative study of both compounds has not been reported so far, and the targets involved in this effect remain unknown. The ability of CBD and CBG to attenuate the neurotoxicity induced by two insults involving oxidative stress (hydrogen peroxide, H2O2) and mitochondrial dysfunction (rotenone) was evaluated in neural cell cultures. The involvement of CB-1 and CB-2 or 5-HT1A receptors was investigated. The neuroprotective effect of their respective acids forms, cannabidiolic acid (CBDA) and cannabigerolic acid (CBGA), was also analyzed. MTT and immunocytochemistry assays were used to evaluate cell viability. No significant variation on cell viability was per se induced by the lower concentrations tested of CBD and CBG or CBDA and CBGA; however, high concentrations of CBD, CBDA, or CBGA were toxic since a 40-50% reduction of cell viability was observed. CBD and CBG showed neuroprotective effects against H2O2 or rotenone; however, both compounds were more effective in attenuating the rotenone-induced neurotoxicity. A high concentration of CBDA reduced the rotenone-induced neurotoxicity. WAY100635 (5-HT1A receptor antagonist) but not AM251 and AM630 (CB1 or CB2 receptor antagonists, respectively) significantly diminished the neuroprotective effect induced by CBG only against rotenone. Our results contribute to the understanding of the neuroprotective effect of CBD and CBG, showing differences with their acid forms, and also highlight the role of 5-HT1A receptors in the mechanisms of action of CBG.
 ...
PMID:A Comparative In Vitro Study of the Neuroprotective Effect Induced by Cannabidiol, Cannabigerol, and Their Respective Acid Forms: Relevance of the 5-HT1A Receptors. 3288 42