PMID- 17699689
OWN - NLM
STAT- MEDLINE
DCOM- 20080108
LR  - 20240312
IS  - 0022-3077 (Print)
IS  - 1522-1598 (Electronic)
IS  - 0022-3077 (Linking)
VI  - 98
IP  - 4
DP  - 2007 Oct
TI  - BDNF induces calcium elevations associated with IBDNF, a nonselective cationic 
      current mediated by TRPC channels.
PG  - 2476-82
AB  - Brain-derived neurotrophic factor (BDNF) has potent actions on hippocampal 
      neurons, but the mechanisms that initiate its effects are poorly understood. We 
      report here that localized BDNF application to apical dendrites of CA1 pyramidal 
      neurons evoked transient elevations in intracellular Ca(2+) concentration, which 
      are independent of membrane depolarization and activation of N-methyl-d-aspartate 
      receptors (NMDAR). These Ca(2+) signals were always associated with I(BDNF), a 
      slow and sustained nonselective cationic current mediated by transient receptor 
      potential canonical (TRPC3) channels. BDNF-induced Ca(2+) elevations required 
      functional Trk and inositol-tris-phosphate (IP(3)) receptors, full intracellular 
      Ca(2+) stores as well as extracellular Ca(2+), suggesting the involvement of TRPC 
      channels. Indeed, the TRPC channel inhibitor SKF-96365 prevented BDNF-induced 
      Ca(2+) elevations and the associated I(BDNF). Thus TRPC channels emerge as novel 
      mediators of BDNF-induced intracellular Ca(2+) elevations associated with 
      sustained cationic membrane currents in hippocampal pyramidal neurons.
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, AL 35294-2182, 
      USA.
FAU - Pozzo-Miller, Lucas
AU  - Pozzo-Miller L
LA  - eng
GR  - P30 NS047466/NS/NINDS NIH HHS/United States
GR  - P30 NS057098/NS/NINDS NIH HHS/United States
GR  - R01 NS40593/NS/NINDS NIH HHS/United States
GR  - P30 HD038985/HD/NICHD NIH HHS/United States
GR  - R01 NS040593/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
DEP - 20070815
PL  - United States
TA  - J Neurophysiol
JT  - Journal of neurophysiology
JID - 0375404
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Calcium Channels)
RN  - 0 (Imidazoles)
RN  - 0 (Inositol 1,4,5-Trisphosphate Receptors)
RN  - 0 (Ion Channels)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - 0 (TRPC Cation Channels)
RN  - EC 2.7.10.1 (Receptor, trkA)
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  - Calcium/*metabolism
MH  - Calcium Channels/drug effects/physiology
MH  - Dendrites/drug effects/physiology
MH  - Electrophysiology
MH  - Hippocampus/cytology/drug effects/physiology
MH  - Imidazoles/pharmacology
MH  - Inositol 1,4,5-Trisphosphate Receptors/physiology
MH  - Ion Channels/drug effects/*physiology
MH  - Organ Culture Techniques
MH  - Patch-Clamp Techniques
MH  - Pyramidal Cells/drug effects/physiology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptor, trkA/metabolism
MH  - Receptors, N-Methyl-D-Aspartate/drug effects/physiology
MH  - TRPC Cation Channels/antagonists & inhibitors/drug effects/*physiology
PMC - PMC2806849
MID - NIHMS166542
EDAT- 2007/08/19 09:00
MHDA- 2008/01/09 09:00
PMCR- 2010/01/14
CRDT- 2007/08/19 09:00
PHST- 2007/08/19 09:00 [pubmed]
PHST- 2008/01/09 09:00 [medline]
PHST- 2007/08/19 09:00 [entrez]
PHST- 2010/01/14 00:00 [pmc-release]
AID - 00797.2007 [pii]
AID - 10.1152/jn.00797.2007 [doi]
PST - ppublish
SO  - J Neurophysiol. 2007 Oct;98(4):2476-82. doi: 10.1152/jn.00797.2007. Epub 2007 Aug 
      15.