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Enhancement of Neurotransmitter Release Induced by Brain-Derived Neurotrophic Factor in Cultured Hippocampal Neurons

Li, Yong-Xin and Zhang, Yinong and Lester, Henry A. and Schuman, Erin M. and Davidson, Norman (1998) Enhancement of Neurotransmitter Release Induced by Brain-Derived Neurotrophic Factor in Cultured Hippocampal Neurons. Journal of Neuroscience, 18 (24). pp. 10231-10240. ISSN 0270-6474. PMCID PMC6793341. doi:10.1523/jneurosci.18-24-10231.1998. https://resolver.caltech.edu/CaltechAUTHORS:20220223-204480000

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Abstract

Brain-derived neurotrophic factor (BDNF), like other neurotrophins, has long-term effects on neuronal survival and differentiation; furthermore, recent work has shown that BDNF also can induce rapid changes in synaptic efficacy. We have investigated the mechanism(s) of these synaptic effects on cultured embryonic hippocampal neurons. In the presence of the GABAA receptor antagonist, picrotoxin, the application of BDNF (100 ng/ml) for 1–5 min increased the amplitude of evoked synaptic currents by 48 ± 9% in 10 of 15 pairs of neurons and increased the frequency of EPSC bursts to 205 ± 20% of the control levels. There was no detectable effect of BDNF on various measures of electrical excitability, including the resting membrane potential, input resistance, action potential threshold, and action potential amplitude. In addition, BDNF did not change the postsynaptic currents induced by the exogenous application of glutamate. BDNF did increase the frequency of miniature EPSCs (mEPSCs) (268.0 ± 46.8% of control frequency), however, without affecting the mEPSC amplitude. The effect of BDNF on mEPSC frequency was blocked by the tyrosine kinase inhibitor K252a and also by the removal of extracellular calcium ([Ca²⁺]ₒ). Fura-2 recordings showed that BDNF elicited an increase in intracellular calcium concentration ([Ca²⁺]꜀). This effect was dependent on [Ca²⁺]ₒ; it was blocked by K252a and by thapsigargin, but not by caffeine. The results demonstrate that BDNF enhances glutamatergic synaptic transmission at a presynaptic locus and that this effect is accompanied by a rise in [Ca²⁺]꜀ that requires the release of Ca²⁺ from IP3-gated stores.


Item Type:Article
Related URLs:
URLURL TypeDescription
https://doi.org/10.1523/JNEUROSCI.18-24-10231.1998DOIArticle
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6793341/PubMed CentralArticle
ORCID:
AuthorORCID
Lester, Henry A.0000-0002-5470-5255
Schuman, Erin M.0000-0002-7053-1005
Additional Information:© 1998 Society for Neuroscience. Received July 29, 1998; revised Sept. 14, 1998; accepted Sept. 17, 1998. This work was supported by the Silvio Conte Center for Neuroscience Research at Caltech sponsored by the National Institute of Mental Health and by Amgen, Thousand Oaks, CA.
Funders:
Funding AgencyGrant Number
Silvio Conte Center for Neuroscience ResearchUNSPECIFIED
AmgenUNSPECIFIED
Subject Keywords:BDNF; calcium; glutamate receptors; hippocampal; neurotrophins; synaptic plasticity; neurotransmitter release
Issue or Number:24
PubMed Central ID:PMC6793341
DOI:10.1523/jneurosci.18-24-10231.1998
Record Number:CaltechAUTHORS:20220223-204480000
Persistent URL:https://resolver.caltech.edu/CaltechAUTHORS:20220223-204480000
Official Citation:Enhancement of Neurotransmitter Release Induced by Brain-Derived Neurotrophic Factor in Cultured Hippocampal Neurons Yong-Xin Li, Yinong Zhang, Henry A. Lester, Erin M. Schuman, Norman Davidson Journal of Neuroscience 15 December 1998, 18 (24) 10231-10240; DOI: 10.1523/JNEUROSCI.18-24-10231.1998
Usage Policy:No commercial reproduction, distribution, display or performance rights in this work are provided.
ID Code:113550
Collection:CaltechAUTHORS
Deposited By: George Porter
Deposited On:24 Feb 2022 16:42
Last Modified:24 Feb 2022 16:42

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