PMID- 17118456
OWN - NLM
STAT- MEDLINE
DCOM- 20070419
LR  - 20240312
IS  - 0163-7258 (Print)
IS  - 0163-7258 (Linking)
VI  - 113
IP  - 2
DP  - 2007 Feb
TI  - Transient receptor potential channels as novel effectors of brain-derived 
      neurotrophic factor signaling: potential implications for Rett syndrome.
PG  - 394-409
AB  - In addition to their prominent role as survival signals for neurons in the 
      developing nervous system, neurotrophins have established their significance in 
      the adult brain as well, where their modulation of synaptic transmission and 
      plasticity may participate in associative learning and memory. These crucial 
      activities are primarily the result of neurotrophin regulation of intracellular 
      Ca(2+) homeostasis and, ultimately, changes in gene expression. Outlined in the 
      following review is a synopsis of neurotrophin signaling with a particular focus 
      upon brain-derived neurotrophic factor (BDNF) and its role in hippocampal 
      synaptic plasticity and neuronal Ca(2+) homeostasis. Neurotrophin signaling 
      through tropomyosin-related kinase (Trk) and pan-neurotrophin receptor 75 kD 
      (p75(NTR)) receptors are also discussed, reviewing recent results that indicate 
      signaling through these two receptor modalities leads to opposing cellular 
      outcomes. We also provide an intriguing look into the transient receptor 
      potential channel (TRPC) family of ion channels as distinctive targets of BDNF 
      signaling; these channels are critical for capacitative Ca(2+) entry, which, in 
      due course, mediates changes in neuronal structure including dendritic spine 
      density. Finally, we expand these topics into an exploration of mental 
      retardation (MR), in particular Rett Syndrome (RTT), where dendritic spine 
      abnormalities may underlie cognitive impairments. We propose that understanding 
      the role of neurotrophins in synapse formation, plasticity, and maintenance will 
      make fundamental contributions to the development of therapeutic strategies to 
      improve cognitive function in developmental disorders associated with MR.
FAU - Amaral, Michelle D
AU  - Amaral MD
AD  - Department of Neurobiology, Civitan International Research Center, McKnight Brain 
      Institute, University of Alabama at Birmingham, Birmingham, AL 35294-2182, USA.
FAU - Chapleau, Christopher A
AU  - Chapleau CA
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  - P30-HD38985/HD/NICHD NIH HHS/United States
GR  - NS40593/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20061121
PL  - England
TA  - Pharmacol Ther
JT  - Pharmacology & therapeutics
JID - 7905840
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (MBD2 protein, human)
RN  - 0 (Transient Receptor Potential Channels)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/*metabolism
MH  - Calcium/metabolism
MH  - DNA-Binding Proteins/metabolism
MH  - Dendritic Spines/pathology
MH  - Humans
MH  - Rett Syndrome/*metabolism/pathology
MH  - Signal Transduction
MH  - Transient Receptor Potential Channels/*metabolism
PMC - PMC1862519
MID - NIHMS18021
EDAT- 2006/11/23 09:00
MHDA- 2007/04/20 09:00
PMCR- 2008/02/03
CRDT- 2006/11/23 09:00
PHST- 2006/09/26 00:00 [received]
PHST- 2006/09/26 00:00 [accepted]
PHST- 2006/11/23 09:00 [pubmed]
PHST- 2007/04/20 09:00 [medline]
PHST- 2006/11/23 09:00 [entrez]
PHST- 2008/02/03 00:00 [pmc-release]
AID - S0163-7258(06)00170-7 [pii]
AID - 10.1016/j.pharmthera.2006.09.005 [doi]
PST - ppublish
SO  - Pharmacol Ther. 2007 Feb;113(2):394-409. doi: 10.1016/j.pharmthera.2006.09.005. 
      Epub 2006 Nov 21.