Evidence map›Paper›PMID 26370162›Full record

ArticleThe European journal of neuroscience2015

Gad1 mRNA as a reliable indicator of altered GABA release from orexigenic neurons in the hypothalamus.

Matthew S Dicken, Alexander R Hughes, Shane T Hentges

Open access · greenAbstract read
In one paragraph

Article in The European journal of neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
1.6field-weighted citation impact, top 20% 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

36 citing papers in PubMed, 54 citations in OpenAlex.

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  8. Abnormal Local Cortical Functional Connectivity due to Interneuron Dysmaturation after Neonatal Intermittent Hypoxia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
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  13. Review
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  15. Article
  16. Seizures regulate the cation-ClFrontiers in neurology · 2023
    Article
  17. Article
  18. Review
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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

3 authors at 1 institution in 1 country.

Matthew S DickenDepartment of Biomedical Sciences, Colorado State University, 1617 Campus Delivery, Fort Collins, CO, 80523, USA.
Alexander R HughesDepartment of Biomedical Sciences, Colorado State University, 1617 Campus Delivery, Fort Collins, CO, 80523, USA.
Shane T HentgesDepartment of Biomedical Sciences, Colorado State University, 1617 Campus Delivery, Fort Collins, CO, 80523, USA.
Colorado State University · US

Funding

Hypothalmic Circuits Regulating Energy Balance and Obesity: Synaptic PhysiologyR01DK078749 · NIDDK · WASHINGTON STATE UNIVERSITY · PI HENTGES, SHANE T · 2008 to 2021
$4.6M
NIDDK NIH HHS R01 DK078749NIDDK NIH HHS R01DK078749
6 · The paper itself

Abstract

The strength of γ-aminobutyric acid (GABA)-mediated inhibitory synaptic input is a principle determinant of neuronal activity. However, because of differences in the number of GABA afferent inputs and the sites of synapses, it is difficult to directly assay for altered GABA transmission between specific cells. The present study tested the hypothesis that the level of mRNA for the GABA synthetic enzyme glutamate decarboxylase (GAD) can provide a reliable proxy for GABA release. This was tested in a mouse hypothalamic circuit important in the regulation of energy balance. Fluorescent in situ hybridization results show that the expression of Gad1 mRNA (encoding the GAD67 enzyme) was increased in hypothalamic neuropeptide Y/agouti-related peptide (NPY/AgRP) neurons after an overnight fast, consistent with the ability of GABA from these neurons to stimulate food intake. Optogenetic studies confirmed that the observed increase in Gad1 mRNA correlated with an increase in the probability of GABA release from NPY/AgRP neurons onto downstream proopiomelanocortin neurons. Likewise, there was an increase in the readily releasable pool of GABA in NPY/AgRP neurons. Selective inhibition of GAD activity in NPY/AgRP neurons decreased GABA release, indicating that GAD67 activity, which is largely dictated by expression level, is a key determinant of GABA release. Altogether, it appears that Gad expression may be a reliable proxy of altered GABAergic transmission. Examining changes in Gad mRNA as a proxy for GABA release may be particularly helpful when the downstream targets are not known or when limited tools exist for detecting GABA release at a particular synapse.

Indexed as

Inhibitory Postsynaptic PotentialsAgouti-Related ProteinAnimalsFastingFemalegamma-Aminobutyric AcidGlutamate DecarboxylaseHypothalamusMaleMiceMice, Inbred C57BLMice, TransgenicNeuronsNeuropeptide YPro-OpiomelanocortinRNA, MessengerAgouti-Related Proteingamma-Aminobutyric AcidGlutamate Decarboxylaseglutamate decarboxylase 1Neuropeptide YPro-OpiomelanocortinRNA, MessengerAgRPin situ hybridizationmouseproopiomelanocortinreadily releasable pool

Identifiers

PMID26370162
PMCPMC4870936
OpenAlexW1844271338

What OpenQuestion holds

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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.