Evidence map›Paper›PMID 9575287›Full record

ArticleThe Journal of physiology1998

Inhibition of N- and P/Q-type calcium channels by postsynaptic GABAB receptor activation in rat supraoptic neurones.

N Harayama, I Shibuya, K Tanaka, N Kabashima, Y Ueta, H Yamashita

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of physiology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

20 citing papers in PubMed, 82 citations in OpenAlex.

  1. Review
  2. Diversity of structure and function of GABAProceedings of the Japan Academy. Series B, Physical and biological sciences · 2018
    Review
  3. Review
  4. Review
  5. Postsynaptic GABAB receptors enhance extrasynaptic GABAA receptor function in dentate gyrus granule cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013
    Article
  6. Review
  7. Article
  8. Article
  9. GABAB receptor activation protects neurons from apoptosis via IGF-1 receptor transactivation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010
    Article
  10. Analgesic alpha-conotoxins Vc1.1 and Rg1A inhibit N-type calcium channels in rat sensory neurons via GABAB receptor activation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008
    Article
  11. Article
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  13. Review
  14. Article
  15. Article
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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

6 authors at 1 institution in 1 country.

N HarayamaDepartment of Physiology, University of Occupational and Environmental Health, School of Medicine, Kitakyushu 807, Japan.
I Shibuya
K Tanaka
N Kabashima
Y Ueta
H Yamashita
University of Occupational and Environmental Health Japan · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

1. Voltage-dependent Ca2+ currents of dissociated rat supraoptic nucleus (SON) neurones were measured using the whole-cell configuration of the patch-clamp technique to examine direct postsynaptic effects of GABAB receptor activation on SON magnocellular neurones. 2. The selective GABAB agonist baclofen reversibly inhibited voltage-dependent Ca2+ currents elicited by voltage steps from a holding potential of -80 mV to depolarized potentials in a dose-dependent manner. The ED50 of baclofen for inhibiting Ca2+ currents was 1.4 x 10-6 M. Baclofen did not inhibit low threshold Ca2+ currents elicited by voltage steps from -120 to -40 mV. 3. Inhibition of high threshold Ca2+ currents by baclofen was rapidly and completely reversed by the selective GABAB antagonists, CGP 35348 and CGP 55845A, when the antagonists were added at the molar ratio vs. baclofen of 10 : 1 and 0.01 : 1, respectively. It was also reversed by a prepulse to +150 mV lasting for 100 ms. 4. The inhibition of Ca2+ currents was abolished when the cells were pretreated with pertussis toxin for longer than 20 h or with N-ethylmaleimide for 2 min. It was also abolished when GDPbetaS was included in the patch pipette. When GTPgammaS was included in the patch pipette, baclofen produced irreversible inhibition of Ca2+ currents and this inhibition was again reversed by the prepulse procedure. 5. The inhibition of N-, P/Q-, L- and R-type Ca2+ channels by baclofen (10-5 M) was 24.1, 10.5, 3.1 and 3. 6 %, respectively, of the total Ca2+ currents. Only the inhibition of N- and P/Q-types was significant. 6. These results suggest that GABAB receptors exist in the postsynaptic sites of the SON magnocellular neurones and mediate selective inhibitory actions on voltage-dependent Ca2+ channels of N- and P/Q-types via pertussis toxin-sensitive G proteins, and that such inhibitory mechanisms may play a role in the regulation of SON neurones by the GABA neurones.

Indexed as

AnimalsBaclofenCalcium Channel BlockersCalcium ChannelsGABA AntagonistsGuanosine DiphosphateIn Vitro TechniquesMaleMembrane PotentialsNeuronsOrganophosphorus CompoundsPatch-Clamp TechniquesPertussis ToxinPhosphinic AcidsPropanolaminesRatsBaclofenCalcium Channel BlockersCalcium ChannelsCGP 35348CGP 55845AGABA Antagonistsguanosine 5'-O-(2-thiodiphosphate)Guanosine DiphosphateOrganophosphorus CompoundsPertussis ToxinPhosphinic AcidsPropanolaminesReceptors, GABA-BThionucleotidesVirulence Factors, Bordetella

Identifiers

PMID9575287
PMCPMC2230969
OpenAlexW2020917920

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.