Journal
JOURNAL OF NEUROPHYSIOLOGY
Volume 98, Issue 4, Pages 2476-2482Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/jn.00797.2007
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Funding
- NICHD NIH HHS [P30 HD038985] Funding Source: Medline
- NINDS NIH HHS [R01 NS040593, P30 NS047466, R01 NS040593-09, P30 NS057098, R01 NS40593] Funding Source: Medline
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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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