BDNF Enhances T-type Ca²⁺ Channel Currents And Increases Membrane Excitability In Small Trigeminal Ganglion Neurons In Rats

Objective:To investigate the possible mechanisms of BDNF on T-type calcium channel currents and excitability in trigeminal ganglion neurons in rats..Methods:Western blot and immunofluorescence was used to identify the expression and distribution of TrkB receptor of the trigeminal ganglion neurons in rats.The whole-cell patch clamp recording was used to investigate the effect of BDNF on T-type calcium channel currents and excitability in small TG neurons.Pharmacological methods was used to clarify its signaling pathways.Results:In the present study,we found that:1)Trk B receptors were expressed in trigeminal ganglion neurons.2)BDNF enhanced T-type Ca⁺channel currents in a dose-dependent manner.BDNF at 50 ng/ml reversibly enhanced T-type Ca⁺channel currents by³0.24%.3)This effect was blocked by Trk B FC chimera,while the GDP-β-S（a selective G protein antagonist）can not block.The effect of BDNF can be blocked by PKI6-22 and KT5720（a selective PKA antagonist）,LY294002（a selective PI3K antagonist）,MK2206（a selective AKT antagonist）,whereas GF109203X（a selective PKC antagonist）have no such effect.4)We observed a siginificant increased firing frequency of action potentials of small TG neurons induced by BDNF,which could be abrogated by pretreatment of the cell with NiCl₂.Conclusions:BDNF enhanced T-type Ca⁺channel currents in a dose-dependent manner.This effect via Trk B receptor,PKA,PI3K/AKT pathway which could contribute to its physiological functions including neuronal excitability.