期刊
JOURNAL OF NEUROSCIENCE
卷 26, 期 52, 页码 13531-13536出版社
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.4576-06.2006
关键词
BDNF; neurosecretion; neurotrophin; synaptic communication; synaptic transmission; synaptogenesis
资金
- NICHD NIH HHS [P01 HD023315, HD23315] Funding Source: Medline
- NINDS NIH HHS [R01 NS041310, NS041310] Funding Source: Medline
Brain-derived neurotrophic factor ( BDNF) is a key regulator of hippocampal synaptic plasticity in the developing and adult nervous system. It can be released from pyramidal neuron dendrites in an activity-dependent manner and has therefore been suggested to serve as a signal that provides the retrograde intercellular communication necessary for Hebbian plasticity and hippocampal-dependent learning. Although much has been learned about BDNF function by field stimulation of hippocampal neurons, it is not known whether moderate action potential-independent depolarization of single cells is capable of releasing sufficient BDNF to influence transmission at individual synapses. In this study, we show directly at the single-cell level that such modulation can occur. By using K-252a, anti-BDNF antibody, and interruption of regulated release, we confirm a model in which postsynaptic depolarization elicits calcium-dependent release of BDNF that diffuses retrogradely and enhances presynaptic transmitter release.
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