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Modulation of neuronal calcium signaling by neurotrophic factors
Author(s) -
McCutchen Mary Eve,
Bramham Clive R.,
PozzoMiller Lucas D.
Publication year - 2002
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/s0736-5748(02)00014-x
Subject(s) - neuroscience , neurotrophic factors , modulation (music) , neurotrophin , microbiology and biotechnology , calcium signaling , signal transduction , brain derived neurotrophic factor , chemistry , calcium , biology , biochemistry , physics , receptor , organic chemistry , acoustics
Brain‐derived neurotrophic factor (BDNF), a member of the neurotrophin (NT) family, is emerging as a key mediator of activity‐dependent modifications of synaptic strength in the central nervous system. Because of the well‐established role of post‐synaptic elevations in concentrations of free Ca 2+ ions ([Ca 2+ ] i ) in synaptic plasticity, we investigated the hypothesis that BDNF exerts its neuromodulatory effects on hippocampal pyramidal neurons by enhancing dendritic [Ca 2+ ] i transients mediated by voltage‐dependent Ca 2+ channels (VDCCs) during the firing of back‐propagating action potentials. Simultaneous whole‐cell recording and microfluorometric Ca 2+ imaging were performed in CA1 pyramidal neurons from hippocampal organotypic slice cultures treated with BDNF for 2–4 days in vitro. Our observations indicate that long‐term exposure to BDNF does not affect [Ca 2+ ] i transients in apical dendrites mediated by influx through L‐type VDCCs during trains of back‐propagating action potentials evoked by direct depolarizing current injections. These results suggest that, despite BDNF's profound effects on hippocampal synaptic plasticity, and of L‐type Ca 2+ channels on neuronal gene transcription, the role of BDNF in cellular models of hippocampus‐dependent learning and memory does not involve modulation of voltage‐gated dendritic Ca 2+ signaling mediated by L‐type channels in apical dendrites of CA1 pyramidal neurons.