5-HT2A receptor activation leads to increased BDNF mRNA expression in C6 glioma cells.

摘要: It has recently been suggested that an increase in brain-derived neurotrophic factor (BDNF) expression may mediate some of the therapeutic effect antidepressant drugs, via their effects on neurotransmitter 5-hydroxytryptamine (5-HT). However, because it is unclear whether 5-HT manipulations directly affect BDNF expression, we examined mRNA levels C6 glioma cells following incubation with using reverse transcription polymerase chain reaction (RT-PCR) and Northern blot analysis. Incubation increased approx twofold. The (100 microM) was inhibited by a 5-HT2A receptor antagonist (ketanserin; 1 microM). RNA synthesis inhibitor (actinomycin D; 10 microg/mL), but not protein (cycloheximide; 0.5 microg/mL) blocked 5-HT. Furthermore, EGTA (1 mM), kinase (staurosporine; microM), Ca2+ ATPase thapsigargin or calcium/calmodulin-dependent (KN 62; response to Our data show increases de novo direct activation receptor, calcium-dependent kinase-dependent pathway.