PMID- 22811938
OWN - NLM
STAT- MEDLINE
DCOM- 20121120
LR  - 20230429
IS  - 1687-5443 (Electronic)
IS  - 2090-5904 (Print)
IS  - 1687-5443 (Linking)
VI  - 2012
DP  - 2012
TI  - Intracellular Ca2+ stores and Ca2+ influx are both required for BDNF to rapidly 
      increase quantal vesicular transmitter release.
PG  - 203536
LID - 10.1155/2012/203536 [doi]
LID - 203536
AB  - Brain-derived neurotrophic factor (BDNF) is well known as a survival factor 
      during brain development as well as a regulator of adult synaptic plasticity. One 
      potential mechanism to initiate BDNF actions is through its modulation of quantal 
      presynaptic transmitter release. In response to local BDNF application to CA1 
      pyramidal neurons, the frequency of miniature excitatory postsynaptic currents 
      (mEPSC) increased significantly within 30 seconds; mEPSC amplitude and kinetics 
      were unchanged. This effect was mediated via TrkB receptor activation and 
      required both full intracellular Ca(2+) stores as well as extracellular Ca(2+). 
      Consistent with a role of Ca(2+)-permeable plasma membrane channels of the TRPC 
      family, the inhibitor SKF96365 prevented the BDNF-induced increase in mEPSC 
      frequency. Furthermore, labeling presynaptic terminals with amphipathic styryl 
      dyes and then monitoring their post-BDNF destaining in slice cultures by 
      multiphoton excitation microscopy revealed that the increase in frequency of 
      mEPSCs reflects vesicular fusion events. Indeed, BDNF application to CA3-CA1 
      synapses in TTX rapidly enhanced FM1-43 or FM2-10 destaining with a time course 
      that paralleled the phase of increased mEPSC frequency. We conclude that BDNF 
      increases mEPSC frequency by boosting vesicular fusion through a presynaptic, 
      Ca(2+)-dependent mechanism involving TrkB receptors, Ca(2+) stores, and TRPC 
      channels.
FAU - Amaral, Michelle D
AU  - Amaral MD
AD  - Department of Neurobiology, Civitan International Research Center, The University 
      of Alabama at Birmingham, SHEL-1002, 1825 University Boulevard, Birmingham, AL 
      35294-2182, USA.
FAU - Pozzo-Miller, Lucas
AU  - Pozzo-Miller L
LA  - eng
GR  - P30 HD038985/HD/NICHD NIH HHS/United States
GR  - R01 NS040593/NS/NINDS NIH HHS/United States
GR  - R01 NS065027/NS/NINDS NIH HHS/United States
GR  - NS-065027/NS/NINDS NIH HHS/United States
GR  - NS40593/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20120703
PL  - United States
TA  - Neural Plast
JT  - Neural plasticity
JID - 100883417
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Calcium Channel Blockers)
RN  - 0 (Imidazoles)
RN  - 0 (Vesicular Neurotransmitter Transport Proteins)
RN  - 4368-28-9 (Tetrodotoxin)
RN  - EC 2.7.10.1 (Receptor, trkB)
RN  - I61V87164A (1-(2-(3-(4-methoxyphenyl)propoxy)-4-methoxyphenylethyl)-1H-imidazole)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/*pharmacology
MH  - CA1 Region, Hippocampal/drug effects/physiology
MH  - Calcium/*metabolism
MH  - Calcium Channel Blockers/pharmacology
MH  - Excitatory Postsynaptic Potentials/drug effects
MH  - Imidazoles/pharmacology
MH  - Kinetics
MH  - Microscopy, Fluorescence
MH  - Organ Culture Techniques
MH  - Patch-Clamp Techniques
MH  - Presynaptic Terminals/drug effects
MH  - Pyramidal Cells/drug effects/physiology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptor, trkB/drug effects
MH  - Stimulation, Chemical
MH  - Tetrodotoxin/pharmacology
MH  - Vesicular Neurotransmitter Transport Proteins/*metabolism
PMC - PMC3397209
EDAT- 2012/07/20 06:00
MHDA- 2012/12/10 06:00
PMCR- 2012/07/03
CRDT- 2012/07/20 06:00
PHST- 2012/04/12 00:00 [received]
PHST- 2012/05/29 00:00 [accepted]
PHST- 2012/07/20 06:00 [entrez]
PHST- 2012/07/20 06:00 [pubmed]
PHST- 2012/12/10 06:00 [medline]
PHST- 2012/07/03 00:00 [pmc-release]
AID - 10.1155/2012/203536 [doi]
PST - ppublish
SO  - Neural Plast. 2012;2012:203536. doi: 10.1155/2012/203536. Epub 2012 Jul 3.