PMID- 25788684
OWN - NLM
STAT- MEDLINE
DCOM- 20150615
LR  - 20181113
IS  - 1529-2401 (Electronic)
IS  - 0270-6474 (Print)
IS  - 0270-6474 (Linking)
VI  - 35
IP  - 11
DP  - 2015 Mar 18
TI  - Brain-derived neurotrophic factor inhibits calcium channel activation, 
      exocytosis, and endocytosis at a central nerve terminal.
PG  - 4676-82
LID - 10.1523/JNEUROSCI.2695-14.2015 [doi]
AB  - Brain-derived neurotrophic factor (BDNF) is a neurotrophin that regulates 
      synaptic function and plasticity and plays important roles in neuronal 
      development, survival, and brain disorders. Despite such diverse and important 
      roles, how BDNF, or more generally speaking, neurotrophins affect synapses, 
      particularly nerve terminals, remains unclear. By measuring calcium currents and 
      membrane capacitance during depolarization at a large mammalian central nerve 
      terminal, the rat calyx of Held, we report for the first time that BDNF slows 
      down calcium channel activation, including P/Q-type channels, and inhibits 
      exocytosis induced by brief depolarization or single action potentials, inhibits 
      slow and rapid endocytosis, and inhibits vesicle mobilization to the readily 
      releasable pool. These presynaptic mechanisms may contribute to the important 
      roles of BDNF in regulating synapses and neuronal circuits and suggest that 
      regulation of presynaptic calcium channels, exocytosis, and endocytosis are 
      potential mechanisms by which neurotrophins achieve diverse neuronal functions.
CI  - Copyright (c) 2015 the authors 0270-6474/15/354676-07$15.00/0.
FAU - Baydyuk, Maryna
AU  - Baydyuk M
AD  - National Institute of Neurological Disorders and Stroke, Bethesda, Maryland 
      20892.
FAU - Wu, Xin-Sheng
AU  - Wu XS
AD  - National Institute of Neurological Disorders and Stroke, Bethesda, Maryland 
      20892.
FAU - He, Liming
AU  - He L
AD  - National Institute of Neurological Disorders and Stroke, Bethesda, Maryland 
      20892.
FAU - Wu, Ling-Gang
AU  - Wu LG
AD  - National Institute of Neurological Disorders and Stroke, Bethesda, Maryland 20892 
      wul@ninds.nih.gov.
LA  - eng
GR  - Intramural NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Intramural
PL  - United States
TA  - J Neurosci
JT  - The Journal of neuroscience : the official journal of the Society for 
      Neuroscience
JID - 8102140
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Calcium Channel Agonists)
SB  - IM
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/*pharmacology
MH  - Calcium Channel Agonists/*pharmacology
MH  - Endocytosis/drug effects/*physiology
MH  - Excitatory Postsynaptic Potentials/drug effects/physiology
MH  - Exocytosis/drug effects/*physiology
MH  - Female
MH  - Male
MH  - Mice, Transgenic
MH  - Organ Culture Techniques
MH  - Presynaptic Terminals/drug effects/*physiology
MH  - Rats
MH  - Rats, Wistar
PMC - PMC4363393
OTO - NOTNLM
OT  - BDNF
OT  - calcium channels
OT  - calyx of Held
OT  - endocytosis
OT  - exocytosis
EDAT- 2015/03/20 06:00
MHDA- 2015/06/16 06:00
PMCR- 2015/09/18
CRDT- 2015/03/20 06:00
PHST- 2015/03/20 06:00 [entrez]
PHST- 2015/03/20 06:00 [pubmed]
PHST- 2015/06/16 06:00 [medline]
PHST- 2015/09/18 00:00 [pmc-release]
AID - 35/11/4676 [pii]
AID - 2695-14 [pii]
AID - 10.1523/JNEUROSCI.2695-14.2015 [doi]
PST - ppublish
SO  - J Neurosci. 2015 Mar 18;35(11):4676-82. doi: 10.1523/JNEUROSCI.2695-14.2015.