Evidence map›Paper›PMID 17204496›Full record

ArticleThe Journal of physiology2007

Reversible inhibition of GABAA receptors by alpha7-containing nicotinic receptors on the vertebrate postsynaptic neurons.

Jingming Zhang, Darwin K Berg

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

44 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Differential Modulation of GABAFrontiers in molecular neuroscience · 2017
    Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Glutamatergic synapse formation is promoted by α7-containing nicotinic acetylcholine receptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    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

2 authors at 1 institution in 1 country.

Jingming ZhangNeurobiology Section, Division of Biological Sciences, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA.
Darwin K Berg
University of California, San Diego · US

Funding

Signal Transduction at Neuronal Nicotinic SynapsesR01NS012601 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BERG, DARWIN K · 1985 to 2016
$5.3M
Nicotinic Control of Non-Nicotinic Synapses in the HippocampusR01NS035469 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BERG, DARWIN K · 1996 to 2013
$4.8M
NINDS NIH HHS NS012601NINDS NIH HHS NS035469NINDS NIH HHS R01 NS012601NINDS NIH HHS R01 NS035469
6 · The paper itself

Abstract

Nicotinic acetylcholine receptors (nAChRs) are expressed throughout the central nervous system and influence a variety of higher order functions including learning and memory. While the effects of presynaptic nAChRs on transmitter release have been well documented, little is known about possible postsynaptic actions. A major species of neuronal nAChRs contains the alpha7 gene product and has a high relative permeability to calcium. Both on rodent hippocampal interneurons and on chick ciliary ganglion neurons these alpha7-nAChRs are often closely juxtaposed to GABAA receptors. We show here that in both cases activation of alpha7-nAChRs on the postsynaptic neuron acutely down-regulates GABA-induced currents. Nicotine application to dissociated ciliary ganglion neurons diminished subsequent GABAA receptor responses to GABA. The effect was blocked by alpha7-nAChR antagonists, by chelation of intracellular Ca2+ with BAPTA, and by inhibition of both Ca2+-calmodulin-dependent protein kinase II and mitogen-activated protein kinase. A similar outcome was obtained in the hippocampus where electrical stimulation to activate cholinergic fibres reduced the amplitude of subsequent GABAA receptor-mediated inhibitory postsynaptic currents. The reduction showed the same calcium and kinase dependence seen in ciliary ganglion neurons and was absent in hippocampal slices from alpha7-nAChR knockout mice. Moreover, alpha7-nAChR blockade in hippocampal slices reduced rundown of GABAA receptor-mediated whole-cell responses, indicating ongoing endogenous modulation. The results demonstrate regulation of GABAA receptors by alpha7-nAChRs on the postsynaptic neuron and identify a new mechanism by which nicotinic cholinergic signalling influences nervous system function.

Indexed as

alpha7 Nicotinic Acetylcholine ReceptorAnimalsCell Culture TechniquesChick EmbryoChickensCholinergic FibersFemalegamma-Aminobutyric AcidGanglia, ParasympatheticHippocampusInhibitory Postsynaptic PotentialsInterneuronsMaleMembrane PotentialsMiceMice, Inbred C57BLalpha7 Nicotinic Acetylcholine ReceptorChrna7 protein, mousegamma-Aminobutyric AcidReceptors, GABA-AReceptors, Nicotinic

Identifiers

PMID17204496
PMCPMC2151364
OpenAlexW1605530892

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.