Evidence map›Paper›PMID 18832421›Full record

ArticleThe Journal of physiology2008

GABA transporter 1 tunes GABAergic synaptic transmission at output neurons of the mouse neostriatum.

Knut Kirmse, Anton Dvorzhak, Sergei Kirischuk, Rosemarie Grantyn

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.2field-weighted citation impact, top 25% 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

26 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. GABA Release from Astrocytes in Health and Disease.International journal of molecular sciences · 2022
    Review
  5. Review
  6. Article
  7. Heterosynaptic GABAThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  8. Inhibition of Nigrostriatal Dopamine Release by Striatal GABAThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  9. Article
  10. Article
  11. Rescue of homeostatic regulation of striatal excitability and locomotor activity in a mouse model of Huntington's disease.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  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

4 authors at 1 institution in 1 country.

Knut KirmseInstitute of Neurophysiology, Johannes Müller Centre of Physiology, Charité - University Medicine Berlin, Tucholskystr. 2, 10117 Berlin, Germany. knut.kirmse@charite.de
Anton Dvorzhak
Sergei Kirischuk
Rosemarie Grantyn
Charité - Universitätsmedizin Berlin · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

GABAergic medium-sized striatal output neurons (SONs) provide the principal output for the neostriatum. In vitro and in vivo data indicate that spike discharge of SONs is tightly controlled by effective synaptic inhibition. Although phasic GABAergic transmission critically depends on ambient GABA levels, the role of GABA transporters (GATs) in neostriatal GABAergic synaptic transmission is largely unknown. In the present study we aimed at elucidating the role of GAT-1 in the developing mouse neostriatum (postnatal day (P) 7-34). We recorded GABAergic postsynaptic currents (PSCs) using the whole-cell patch-clamp technique. Based on the effects of NO-711, a specific GAT-1 blocker, we demonstrate that GAT-1 is operative at this age and influences GABAergic synaptic transmission by presynaptic and postsynaptic mechanisms. Presynaptic GABA(B)R-mediated suppression of GABA release was found to be functional at all ages tested; however, there was no evidence for persistent GABA(B)R activity under control conditions, unless GAT-1 was blocked (P12-34). In addition, whereas no tonic GABA(A)R-mediated conductances were detected in SONs until P14, application of a specific GABA(A)R antagonist caused distinct tonic outward currents later in development (P19-34). In the presence of NO-711, tonic GABA(A)R-mediated currents were also observed at P7-14 and were dramatically increased at more mature stages. Furthermore, GAT-1 block reduced the median amplitude of GABAergic miniature PSCs indicating a decrease in quantal size. We conclude that in the murine neostriatum GAT-1 operates in a net uptake mode. It prevents the persistent activation of presynaptic GABA(B)Rs (P12-34) and prevents (P7-14) or reduces (P19-34) tonic postsynaptic GABA(A)R activity.

Indexed as

Action PotentialsAnimalsAnimals, NewbornBaclofenBicucullineElectric ImpedanceElectric StimulationElectrophysiologyGABA AntagonistsGABA-A Receptor AntagonistsGABA-B Receptor AntagonistsIn Vitro TechniquesMembrane PotentialsMiceMice, Inbred C57BLNeostriatumBaclofenBicucullinebicuculline methiodideCGP 55845AGABA AntagonistsGABA-A Receptor AntagonistsGABA-B Receptor AntagonistsgabazineNipecotic AcidsNNC 711OximesPhosphinic AcidsPropanolaminesPyridazinesReceptors, GABAReceptors, GABA-AReceptors, GABA-BTetrodotoxin

Identifiers

PMID18832421
PMCPMC2655402
OpenAlexW2143933349

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.