Extensive evidence suggests that BDNF regulates neural function and architecture after depolarization. Expression of BDNF is increased after depolarization, and the ability of BDNF to modulate synaptic function is well documented. To further investigate BDNF signaling after activity, we analyzed the effects of depolarization or BDNF treatment on receptor mRNA expression in cultured basal forebrain neurons. Levels of mRNA coding for the cognate BDNF receptor, trkB, as well as the common neurotrophin receptor, p75, were quantitated simultaneously using a sensitive solution hybridization technique. Depolarization or BDNF treatment increased p75 mRNA expression 94% and 195%, respectively. In contrast, trkB message decreased 23% after depolarization but was unchanged by BDNF treatment. Together, these changes resulted in significant increases in the p75/trkB ratio after depolarization or BDNF treatment that could alter BDNF binding or signal transduction.