Evidence map›Paper›PMID 22238092›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012

GABA is excitatory in adult vasopressinergic neuroendocrine cells.

Juhee Haam, Ion R Popescu, Linda A Morton, Katalin C Halmos, Ryoichi Teruyama, Yoichi Ueta, Jeffrey G Tasker

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
10.6field-weighted citation impact, top 2% 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

49 citing papers in PubMed, 105 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Evidence for Two Subpopulations of Cerebrospinal Fluid-Contacting Neurons with Opposite GABAergic Signaling in Adult Mouse Spinal Cord.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  5. Article
  6. Article
  7. Article
  8. Frontiers in psychiatry · 2023
    Review
  9. Article
  10. Article
  11. Review
  12. Review
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  14. Article
  15. Article
  16. Article
  17. Tonic GABAThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    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

7 authors at 3 institutions in 2 countries.

Juhee HaamDepartment of Cell and Molecular Biology, Tulane University, New Orleans, Louisiana 70118, USA.
Ion R Popescu
Linda A Morton
Katalin C Halmos
Ryoichi Teruyama
Yoichi Ueta
Jeffrey G Tasker
Tulane University · USLouisiana State University · USUniversity of Occupational and Environmental Health Japan · JP

Funding

Synaptic Plasticity of Hypothalamic NeuronsR01NS042081 · NINDS · TULANE UNIVERSITY OF LOUISIANA · PI TASKER, JEFFREY G · 2003 to 2008
$1.9M
NINDS NIH HHS NS042081NINDS NIH HHS R01 NS042081
6 · The paper itself

Abstract

Neuronal excitability in the adult brain is controlled by a balance between synaptic excitation and inhibition mediated by glutamate and GABA, respectively. While generally inhibitory in the adult brain, GABA(A) receptor activation is excitatory under certain conditions in which the GABA reversal potential is shifted positive due to intracellular Cl(-) accumulation, such as during early postnatal development and brain injury. However, the conditions under which GABA is excitatory are generally either transitory or pathological. Here, we reveal GABAergic synaptic inputs to be uniformly excitatory in vasopressin (VP)-secreting magnocellular neurons in the adult hypothalamus under normal conditions. The GABA reversal potential (E(GABA)) was positive to resting potential and spike threshold in VP neurons, but not in oxytocin (OT)-secreting neurons. The VP neurons lacked expression of the K(+)-Cl(-) cotransporter 2 (KCC2), the predominant Cl(-) exporter in the adult brain. The E(GABA) was unaffected by inhibition of KCC2 in VP neurons, but was shifted positive in OT neurons, which express KCC2. Alternatively, inhibition of the Na(+)-K(+)-Cl(-) cotransporter 1 (NKCC1), a Cl(-) importer expressed in most cell types mainly during postnatal development, caused a negative shift in E(GABA) in VP neurons, but had no effect on GABA currents in OT neurons. GABA(A) receptor blockade caused a decrease in the firing rate of VP neurons, but an increase in firing in OT neurons. Our findings demonstrate that GABA is excitatory in adult VP neurons, suggesting that the classical excitation/inhibition paradigm of synaptic glutamate and GABA control of neuronal excitability does not apply to VP neurons.

Indexed as

AgingAnimalsExcitatory Postsynaptic PotentialsGABAergic Neuronsgamma-Aminobutyric AcidMaleNeuroendocrine CellsParaventricular Hypothalamic NucleusRatsRats, TransgenicRats, WistarSupraoptic NucleusVasopressinsgamma-Aminobutyric AcidVasopressins

Identifiers

PMID22238092
PMCPMC3561926
OpenAlexW1965453664

What OpenQuestion holds

Textmetadata
LicenceTDM
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.