ArticleThe international journal of neuropsychopharmacology2010
Reduced level of glutamic acid decarboxylase-67 kDa in the prefrontal cortex in major depression.
Article in The international journal of neuropsychopharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers, 3 of them syntheses that pooled it.
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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.
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Who cites it
104 citing papers in PubMed, 3 syntheses or guidelines pooled it, 195 citations in OpenAlex.
- Brain-wide changes in excitation-inhibition balance of major depressive disorder: a systematic review of topographic patterns of GABA- and glutamatergic alterations.Molecular psychiatry · 2023Pooled it
- Medial Frontal Cortex GABA Concentrations in Psychosis Spectrum and Mood Disorders: A Meta-analysis of Proton Magnetic Resonance Spectroscopy Studies.Biological psychiatry · 2023Pooled it
- Human Dermal Fibroblast: A Promising Cellular Model to Study Biological Mechanisms of Major Depression and Antidepressant Drug Response.Current neuropharmacology · 2020Pooled it
- Imbalance in excitation and inhibition in sgACC is associated with depression in dementia with Lewy bodies.Translational psychiatry · 2026Article
- A Comparison of Positive and Negative Allosteric Modulators of α5-Containing GABABiological psychiatry · 2026Review
- Treadmill exercise relieves cortical interneuron hyperactivation to prevent stress-induced anxiety-like behaviors in male mice.Communications biology · 2026Article
- The synaptic triad in depression: how stress-related pathways converge on BDNF, NMDA receptor, and MMP-9.Pharmacological reports : PR · 2026Review
- Deep Brain Stimulation of Lateral Habenula Ameliorates Depression-like Symptoms in Rats: Involvement of Mesolimbic Circuit.Neurochemical research · 2026Article
- Esketamine ameliorates depression-like behavior in mice via modulation of the NRG1-ErbB4 pathway.Frontiers in psychiatry · 2026Article
- Propofol for depression: mechanisms and therapeutic potential.Frontiers in physiology · 2026Review
- Can Sodium Oxybate Mitigate the Symptoms of Schizophrenia?Current neuropharmacology · 2026Review
- Dynamic Behavioral and Molecular Changes Induced by Chronic Restraint Stress Exposure in Mice.International journal of molecular sciences · 2025Article
- Rapid-acting NMDA and GABAergic Modulators in Mood Disorders: From Synaptic Mechanisms to Clinical Practice.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2025Review
- Antidepressant effects of fluoxetine: upregulation of connexin 36 and 43 in the hippocampus, prefrontal cortex, and amygdala.Molecular biology reports · 2025Article
- A Refined Approach to Isolate Interneurons for High-Validity Epigenetic Studies in Human Brain Tissue.Methods and protocols · 2025Article
- Prefrontal Internal Event-Driven Analysis of Dynamical Electroencephalographic Biomarkers in Depression During Emotional Auditory Task.CNS neuroscience & therapeutics · 2025Article
- Effects of ketamine on GABAergic and glutamatergic activity in the mPFC: biphasic recruitment of GABA function in antidepressant-like responses.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025Article
- Ciprofol Alleviates Depressive-Like Behaviors in CUMS Mice Through PPARα-Associated ERK/CREB Signaling Activation.Drug design, development and therapy · 2025Article
- Brain functional alterations in early stage of coal workers' pneumoconiosis with alcoholism: insights from a resting-state fMRI investigation.Frontiers in neuroscience · 2025Article
- Decreased prefrontal glutamatergic function is associated with a reduced astrocyte-related gene expression in treatment-resistant depression.Translational psychiatry · 2024Article
44 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Accumulating evidence suggests dysfunction of the gamma-aminobutyric acid (GABA) system in major depressive disorder (MDD). Neuroimaging studies consistently report reductions of cortical GABA in depressed patients. Our post-mortem analyses demonstrate a reduction in the density and size of GABAergic interneurons in the dorsolateral prefrontal cortex (DLPFC) in MDD. The goal of this study was to test whether the level of glutamic acid decarboxylase (GAD), the GABA synthesizing enzyme, will also be reduced in the same cortical region in MDD. Levels of GAD-65 and GAD-67 proteins were investigated by Western blotting in samples from the DLPFC (BA 9) in 13 medication-free subjects with MDD, and 13 psychiatrically healthy controls. The overall amount of GAD-67 was significantly reduced (-34%) in depressed subjects compared to matched controls. Since recent neuroimaging studies have demonstrated that antidepressants modulate GABA levels, additional experiments were performed to examine the levels of GAD in eight depressed subjects treated with antidepressant medications. Levels of GAD-67 were unchanged in these depressed subjects compared to their respective controls (n=8). The overall amounts of GAD-65 were similar in depressed subjects compared to matched controls, regardless of antidepressant medication. Reduced levels of GAD-67, which is localized to somata of GABA neurons, further support our observation of a decreased density of GABAergic neurons in the PFC in depression. It is likely that a decrease in GAD-67 accounts for the reduction in GABA levels revealed by neuroimaging studies. Moreover, our data support previous neuroimaging observations that antidepressant medication normalizes GABA deficits in depression.
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Registered trials
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 Socratic graph.