PMID- 17494704
OWN - NLM
STAT- MEDLINE
DCOM- 20070622
LR  - 20181113
IS  - 1529-2401 (Electronic)
IS  - 0270-6474 (Print)
IS  - 0270-6474 (Linking)
VI  - 27
IP  - 19
DP  - 2007 May 9
TI  - TRPC3 channels are necessary for brain-derived neurotrophic factor to activate a 
      nonselective cationic current and to induce dendritic spine formation.
PG  - 5179-89
AB  - Brain-derived neurotrophic factor (BDNF) exerts prominent effects on hippocampal 
      neurons, but the mechanisms that initiate its actions are poorly understood. We 
      report here that BDNF evokes a slowly developing and sustained nonselective 
      cationic current (I(BDNF)) in CA1 pyramidal neurons. These responses require 
      phospholipase C, IP3 receptors, Ca2+ stores, and Ca2+ influx, suggesting the 
      involvement of transient receptor potential canonical subfamily (TRPC) channels. 
      Indeed, I(BDNF) is absent after small interfering RNA-mediated TRPC3 knockdown. 
      The sustained kinetics of I(BDNF) appears to depend on phosphatidylinositol 
      3-kinase-mediated TRPC3 membrane insertion, as shown by surface biotinylation 
      assays. Slowly emerging membrane currents after theta burst stimulation are 
      sensitive to the scavenger TrkB-IgG and TRPC inhibitors, suggesting I(BDNF) 
      activation by evoked released of endogenous, native BDNF. Last, TRPC3 channels 
      are necessary for BDNF to increase dendritic spine density. Thus, TRPC channels 
      emerge as novel mediators of BDNF-mediated dendritic remodeling through the 
      activation of a slowly developing and sustained membrane depolarization.
FAU - Amaral, Michelle D
AU  - Amaral MD
AD  - Department of Neurobiology, Civitan International Research Center and McKnight 
      Brain Institute, University of Alabama at Birmingham, Birmingham, Alabama 35294, 
      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  - P30-HD38985/HD/NICHD NIH HHS/United States
GR  - R01-NS40593/NS/NINDS NIH HHS/United States
GR  - R01 NS040593-09/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
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 (Inositol 1,4,5-Trisphosphate Receptors)
RN  - 0 (TRPC Cation Channels)
RN  - 0 (TRPC3 cation channel)
RN  - EC 2.7.10.1 (Receptor, trkB)
RN  - EC 3.1.4.- (Type C Phospholipases)
SB  - IM
MH  - Animals
MH  - Animals, Newborn
MH  - Brain-Derived Neurotrophic Factor/*metabolism/pharmacology
MH  - Calcium Signaling/physiology
MH  - Cell Differentiation/drug effects/physiology
MH  - Dendritic Spines/drug effects/*metabolism/ultrastructure
MH  - Down-Regulation/drug effects/physiology
MH  - Hippocampus/*growth & development/*metabolism/ultrastructure
MH  - Inositol 1,4,5-Trisphosphate Receptors/metabolism
MH  - Membrane Potentials/drug effects/physiology
MH  - Neuronal Plasticity/drug effects/physiology
MH  - Organ Culture Techniques
MH  - Pyramidal Cells/*metabolism/ultrastructure
MH  - RNA Interference
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptor, trkB/metabolism
MH  - TRPC Cation Channels/drug effects/genetics/*metabolism
MH  - Type C Phospholipases/metabolism
PMC - PMC2806846
MID - NIHMS166550
EDAT- 2007/05/15 09:00
MHDA- 2007/06/23 09:00
PMCR- 2007/11/09
CRDT- 2007/05/15 09:00
PHST- 2007/05/15 09:00 [pubmed]
PHST- 2007/06/23 09:00 [medline]
PHST- 2007/05/15 09:00 [entrez]
PHST- 2007/11/09 00:00 [pmc-release]
AID - 27/19/5179 [pii]
AID - 3205451 [pii]
AID - 10.1523/JNEUROSCI.5499-06.2007 [doi]
PST - ppublish
SO  - J Neurosci. 2007 May 9;27(19):5179-89. doi: 10.1523/JNEUROSCI.5499-06.2007.