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BDNF Induces Calcium Elevations Associated With I_BDNF, a Nonselective Cationic Current Mediated by TRPC Channels

Department of Neurobiology, Civitan International Research Center and McKnight Brain Institute, University of Alabama at Birmingham, Birmingham, Alabama

Submitted 16 July 2007; accepted in final form 9 August 2007

Brain-derived neurotrophic factor (BDNF) has potent actions on hippocampal neurons, but the mechanisms that initiate its effects are poorly understood. We report here that localized BDNF application to apical dendrites of CA1 pyramidal neurons evoked transient elevations in intracellular Ca²⁺ concentration, which are independent of membrane depolarization and activation of N-methyl-D-aspartate receptors (NMDAR). These Ca²⁺ signals were always associated with I_BDNF, a slow and sustained nonselective cationic current mediated by transient receptor potential canonical (TRPC3) channels. BDNF-induced Ca²⁺ elevations required functional Trk and inositol-tris-phosphate (IP₃) receptors, full intracellular Ca²⁺ stores as well as extracellular Ca²⁺, suggesting the involvement of TRPC channels. Indeed, the TRPC channel inhibitor SKF-96365 prevented BDNF-induced Ca²⁺ elevations and the associated I_BDNF. Thus TRPC channels emerge as novel mediators of BDNF-induced intracellular Ca²⁺ elevations associated with sustained cationic membrane currents in hippocampal pyramidal neurons.

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