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Brain‐derived neurotrophic factor induces long‐lasting Ca 2+ ‐activated K + currents in rat visual cortex neurons
Author(s) -
Mizoguchi Yoshito,
Monji Akira,
Nabekura Junichi
Publication year - 2002
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.1460-9568.2002.02198.x
Subject(s) - apamin , intracellular , brain derived neurotrophic factor , neuroscience , reversal potential , chemistry , medicine , neurotransmission , postsynaptic potential , phospholipase c , trk receptor , neurotrophic factors , biophysics , endocrinology , biology , patch clamp , microbiology and biotechnology , calcium , receptor , electrophysiology
Brain‐derived neurotrophic factor (BDNF) increases postsynaptic intracellular Ca 2+ and modulates synaptic transmission in various types of neurons. Ca 2+ ‐activated K + currents, opened mainly by intracellular Ca 2+ elevation, contribute to hyperpolarization following action potentials and modulate synaptic transmission. We asked whether BDNF induces Ca 2+ ‐activated K + currents by postsynaptic elevation of intracellular Ca 2+ in acutely dissociated visual cortex neurons of rats. Currents were analysed using the nystatin‐perforated patch clamp technique and imaging of intracellular Ca 2+ mobilization with fura‐2. At a holding potential of −50 mV, BDNF application (20 ng/mL) for 1–2 min induced an outward current (I BDNF‐OUT; 80.0 ± 29.0 pA) lasting for more than 90 min without attenuation in every neuron tested. K252a (200 n m ), an inhibitor of Trk receptor tyrosine kinase, and U73122 (3 μ m ), a specific phospholipase C (PLC)‐γ inhibitor, suppressed I BDNF‐OUT completely. I BDNF‐OUT was both charybdotoxin‐ (600 n m ) and apamin‐ (300 n m ) sensitive, suggesting that this current was carried by Ca 2+ ‐activated K + channels. BAPTA‐AM (150 μ m ) gradually suppressed I BDNF‐OUT . Fura‐2 imaging revealed that a brief application of BDNF elicited a long‐lasting elevation of intracellular Ca 2+ . These results show that BDNF induces long‐lasting Ca 2+ ‐activated K + currents by sustained intracellular Ca 2+ elevation in rat visual cortex neurons. While BDNF, likely acting through the Trk B receptor, was necessary for the induction of long‐lasting Ca 2+ ‐activated K + currents via intracellular Ca 2+ elevation, BDNF was not necessary for the maintenance of this current.