Evidence map›Paper›PMID 10493768›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1999

Decreased G-protein-mediated regulation and shift in calcium channel types with age in hippocampal cultures.

E M Blalock, N M Porter, P W Landfield

Abstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1999. 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
–field-weighted citation impact
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.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Disrupting function of FK506-binding protein 1b/12.6 induces the Ca²+-dysregulation aging phenotype in hippocampal neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Normal brain ageing: models and mechanisms.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2005
    Review
  17. Article
  18. Gene microarrays in hippocampal aging: statistical profiling identifies novel processes correlated with cognitive impairment.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003
    Article
  19. Article
  20. Vitamin D hormone confers neuroprotection in parallel with downregulation of L-type calcium channel expression in hippocampal neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2001
    Article
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.

E M BlalockDepartment of Pharmacology, College of Medicine, University of Kentucky, Lexington, Kentucky 40536, USA.
N M Porter
P W Landfield

Funding

ROLE OF CALCIUM, CALPAINS, AND CASPASES IN NEURODEGENERATIONP01AG010836 · NIA · UNIVERSITY OF KENTUCKY · PI LANDFIELD, PHILIP W. · 1992 to 2008
$12.4M
HIPPOCAMPAL SYNAPTIC STRUCTURE--PHYSIOLOGY DURING AGINGR37AG004542 · NIA · UNIVERSITY OF KENTUCKY · PI LANDFIELD, PHILIP W. · 1998 to 2020
$7.1M
HIPPOCAMPAL SYNAPTIC STUCTURE-PHYSIOLOGY DURING AGINGR01AG004542 · NIA · WAKE FOREST UNIVERSITY · PI LANDFIELD, PHILIP W. · 1985 to 1995
–
NIA NIH HHS AG04542NIA NIH HHS AG10836NIA NIH HHS P01 AG010836NIA NIH HHS R37 AG004542
6 · The paper itself

Abstract

The membrane density of L-type voltage-sensitive Ca(2+) channels (L-VSCCs) of rat hippocampal neurons increases over age [days in vitro (DIV)] in long-term primary cultures, apparently contributing both to spontaneous cell death and to enhanced excitotoxic vulnerability. Similar increases in L-VSCCs occur during brain aging in vivo in rat and rabbit hippocampal neurons. However, unraveling both the molecular basis and the functional implications of these age changes in VSCC density will require determining whether the other types of high-threshold VSCCs (e.g., N, P/Q, and R) also exhibit altered density and/or changes in regulation, for example, by the important G-protein-coupled, membrane-delimited inhibitory pathway. These possibilities were tested here in long-term hippocampal cultures. Pharmacologically defined whole-cell currents were corrected for cell size differences over age by normalization with whole-cell capacitance. The Ca(2+) channel current density (picoamperes per picofarad), mediated by each Ca(2+) channel type studied here (L, N, and a combined P/Q + R component), increased through 7 DIV. Thereafter, however, only L-type current density continued to increase, at least through 21 DIV. Concurrently, pertussis toxin-sensitive G-protein-coupled inhibition of non-L-type Ca(2+) channel current induced by the GABA(B) receptor agonist baclofen or by guanosine 5'-3-O-(thio)triphosphate declined dramatically with age in culture. Thus, the present studies identify selective and novel parallel mechanisms for the time-dependent alteration of Ca(2+) influx, which could importantly influence function and vulnerability during development and/or aging.

Indexed as

AnimalsBaclofenCalcium ChannelsCalcium Channels, L-TypeCell DivisionCells, CulturedCellular SenescenceFetusGABA-B Receptor AgonistsGTP-Binding ProteinsGuanosine 5'-O-(3-Thiotriphosphate)HippocampusNeuronsNimodipineomega-Conotoxin GVIAPatch-Clamp TechniquesBaclofenCalcium ChannelsCalcium Channels, L-TypeGABA-B Receptor AgonistsGTP-Binding ProteinsGuanosine 5'-O-(3-Thiotriphosphate)Nimodipineomega-Conotoxin GVIAPeptidesTetrodotoxin

Identifiers

PMID10493768
PMCPMC6783042

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.