Evidence map›Paper›PMID 17118456›Full record

ReviewPharmacology & therapeutics2007

Transient receptor potential channels as novel effectors of brain-derived neurotrophic factor signaling: potential implications for Rett syndrome.

Michelle D Amaral, Christopher A Chapleau, Lucas Pozzo-Miller

Abstract readReview
In one paragraph

Review in Pharmacology & therapeutics, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.3field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 48 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. BDNF deregulation in Rett syndrome.Neuropharmacology · 2014
    Review
  6. Review
  7. Review
  8. Article
  9. Nanoparticle-mediated signaling endosome localization regulates growth cone motility and neurite growth.Proceedings of the National Academy of Sciences of the United States of America · 2011
    Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Michelle D AmaralDepartment of Neurobiology, Civitan International Research Center, McKnight Brain Institute, University of Alabama at Birmingham, Birmingham, AL 35294-2182, USA.
Christopher A Chapleau
Lucas Pozzo-Miller
University of Alabama at Birmingham · USCivitan International · US

Funding

UAB MENTAL RETARDATION RESEARCH CENTER (MRRC)P30HD038985 · NICHD · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BRENNER, MICHAEL · 2000 to 2012
$8.6M
ACTIONS OF BDNF ON CA2+ SIGNALS IN HIPPOCAMPAL NEURONSR01NS040593 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI POZZO-MILLER, LUCAS D · 2000 to 2010
$2.8M
MeCP2 Modulation of BDNF Signaling: Shared Mechanisms of Rett and AutismR01NS065027 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI POZZO-MILLER, LUCAS D · 2010 to 2014
$1.7M
NICHD NIH HHS P30 HD038985NICHD NIH HHS P30-HD38985NINDS NIH HHS NS40593NINDS NIH HHS R01 NS040593NINDS NIH HHS R01 NS065027
6 · The paper itself

Abstract

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.

Indexed as

AnimalsBrain-Derived Neurotrophic FactorCalciumDendritic SpinesDNA-Binding ProteinsHumansRett SyndromeSignal TransductionTransient Receptor Potential ChannelsBrain-Derived Neurotrophic FactorCalciumDNA-Binding ProteinsMBD2 protein, humanTransient Receptor Potential Channels

Identifiers

PMID17118456
PMCPMC1862519
OpenAlexW2077936590

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.