GABA-related transcripts in the dorsolateral prefrontal cortex in mood disorders
Open accessAbstract
Reduced cortical γ-aminobutyric acid (GABA) levels and altered markers for subpopulations of GABA interneurons have been reported in major depressive disorder (MDD) by in-vivo brain imaging and post-mortem histological studies. Subgroups of GABA interneurons exert differential inhibitory control on principal pyramidal neurons and can be identified based on the non-overlapping expression of the calcium-binding proteins parvalbumin (PV) or calretinin (CR) or the neuropeptide somatostatin (SST). As altered markers of GABAergic functions may also be present in bipolar disorder (BPD), the specificity of particular GABA-related molecular deficits in mood disorders is not known. We used real-time quantitative polymerase chain reaction (qPCR) to assess expression levels of two GABA synthesizing enzymes (glutamate decarboxylase; GAD65 and GAD67) and of three markers of GABA neuron subpopulations (PV, CR, SST) in the dorsolateral prefrontal cortex (DLPFC; Brodmann area 9) in triads (n=19) of control subjects and matched subjects with BPD or MDD. BPD subjects demonstrated significantly reduced PV mRNA, trend level reduction in SST mRNA and no alterations in GAD67, GAD65, or CR mRNA levels; MDD subjects demonstrated reduced SST mRNA expression without alterations in the other transcripts. The characteristic age-related decline in SST expression was not observed in MDD, as low expression was detected across age in MDD subjects. After controlling for age, MDD subjects demonstrated significantly reduced SST mRNA expression. Decreased SST levels in MDD were confirmed at the protein precursor level. Results were not explained by other clinical, demographic or technical parameters. In summary, MDD was characterized by low DLPFC SST, whereas decreased PV mRNA appears to distinguish BPD from MDD.
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GABAergic signaling is decreased in regions comprising the default mode network, while it is increased in the lateral prefrontal cortex.
“Meanwhile, GABAergic signaling is decreased in regions comprising the default mode network (DMN), while it is increased in the lateral prefrontal cortex (LPFC). 212 , 213”
From Major depressive disorder: hypothesis, mechanism, prevention and treatment (2024) · cites this paper as [213]
The Introduction reports decreased GABA content in occipital and frontal cortices in major depressive disorder, which supports a general decrease but does not identify default mode network regions. The Abstract and Results report reduced GABA-related markers in the dorsolateral prefrontal cortex, not increased signaling there; the study measured transcripts rather than signaling directly. (LLM, conf=0.85)
Experimental — accuracy not yet measuredThe SST mRNA level is specifically decreased in patients with MDD.
“and the SST mRNA level is specifically decreased in patients with MDD. 213”
From Major depressive disorder: hypothesis, mechanism, prevention and treatment (2024) · cites this paper as [213]
In “Alterations in GABA-related transcripts across subject groups,” SST mRNA was significantly lower in MDD than in controls after accounting for age. The word “specifically” overstates the distinction from BPD: BPD showed a nonsignificant downward trend, and SST mRNA did not differ significantly between the MDD and BPD groups. (LLM, conf=0.85)
Experimental — accuracy not yet measuredLoss of SST transcript and SST-related synaptic deficits have been identified in the dlPFC of patients suffering from schizophrenia.
“Loss of SST transcript and SST-related synaptic deficits have been identified in the dlPFC of patients suffering from schizophrenia.67,68,69”
From Uncovering the signatures of aging and senescence in the human dorsolateral prefrontal cortex (2026) · cites this paper as [69]
The Discussion reports robust reductions in SST mRNA in subjects with schizophrenia. The ‘SST in age and disease’ section proposes possible effects of low SST on neural and synaptic development, but does not report identified SST-related synaptic deficits in the dlPFC of those patients. Page numbers are unavailable in our copy. (LLM, conf=0.86)
Experimental — accuracy not yet measuredSST transcript decline and SST+ neuron density loss have been implicated in various neurological diseases and disorders.
“both of which have been implicated in various neurological diseases and disorders.”
From Uncovering the signatures of aging and senescence in the human dorsolateral prefrontal cortex (2026) · cites this paper as [69]
The 'Decreased SST in MDD' section links reduced SST mRNA expression to major depressive disorder, and 'SST in age and disease' discusses a possible link between low SST and altered mood regulation. The paper does not establish a loss of SST-positive neuron density; its Introduction describes reduced density of calbindin-immunoreactive interneurons, which is not the same measure. (LLM, conf=0.87)
Experimental — accuracy not yet measuredInterneuron markers and interneuron-associated transcripts are decreased in the prefrontal cortex and anterior cingulate cortex in human MDD brain tissue and chronically stressed rats.
“Immunohistochemical analysis of interneurons and transcripts of interneuron-associated proteins are decreased within the PFC and anterior cingulate cortex in human MDD brain tissue and in chronically stressed rats, suggesting that deficits in GABA levels may contribute to the symptoms of depression [205][206][207][208].”
From Plasticity of synapses and reward circuit function in the genesis and treatment of depression (2023) · cites this paper as [206]
GABA deficits may contribute to depression symptoms.
“Immunohistochemical analysis of interneurons and transcripts of interneuron-associated proteins are decreased within the PFC and anterior cingulate cortex in human MDD brain tissue and in chronically stressed rats, suggesting that deficits in GABA levels may contribute to the symptoms of depression [205][206][207][208].”
From Plasticity of synapses and reward circuit function in the genesis and treatment of depression (2023) · cites this paper as [206]
Decreases in SST expression are detected in the dorsolateral prefrontal cortex and subgenual anterior cingulate cortex of depressed patients and the prefrontal cortex of mice exposed to chronic unpredictable stress.
“Decreases in SST expression are detected in the dorsolateral prefrontal cortex and subgenual anterior cingulate cortex of depressed patients as well as the prefrontal cortex of mice exposed to chronic unpredictable stress, while changes in PV are less consistent [134-136].”
From An emerging circuit pharmacology of GABAA receptors (2018) · cites this paper as [134]
Changes in PV expression are less consistent.
“Decreases in SST expression are detected in the dorsolateral prefrontal cortex and subgenual anterior cingulate cortex of depressed patients as well as the prefrontal cortex of mice exposed to chronic unpredictable stress, while changes in PV are less consistent [134-136].”
From An emerging circuit pharmacology of GABAA receptors (2018) · cites this paper as [134]
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The Role of Genetic Sex in Affect Regulation and Expression of GABA-Related Genes Across Species
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Self-citationSustained Molecular Pathology Across Episodes and Remission in Major Depressive Disorder
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Uncovering the signatures of aging and senescence in the human dorsolateral prefrontal cortex
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“69 In our previous work, we found that SST transcript was reduced in gray-matter layers 1–6 comparing ALS-FTD patients with and without cognitive impairment to nonpathological controls.”
- Authors
- Sibille, E., Morris, H. M., Kota, R. S., & Lewis, D. A.
- Affiliations
- University of Pittsburgh (US)
- Corresponding author
- Sibille, Etienne
- Venue
- International Journal of Neuropsychopharmacology
- Publisher
- Oxford University Press (OUP)
- Published
- 2011-07
- Volume
- 14
- Issue
- 6
- Pages
- 721-734
- ISSN
- 1461-1457 (ISSN-L)
- 1469-5111
- PMC
- PMC3388740
- OpenAlex
- W2153973179
- Cited by
- 217
- References
- 60
- Citations by year
- 2026: 10 · 2025: 4 · 2024: 12 · 2023: 16 · 2022: 12 · 2021: 20 · 2020: 18 · 2019: 25 · 2018: 10 · 2017: 10 · 2016: 16 · 2015: 17 · 2014: 20 · 2013: 12 · 2012: 7
- FWCI
- 10.54
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The International Journal of Neuropsychopharmacology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (MH077159, MH45156)
- National Institute of Mental Health (MH084060, MH 45156, MH077159, R01MH067234, R01MH077159, P50MH045156, K02MH084060, R01MH079299)
- Topics
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Health Sciences › Medicine › Psychiatry and Mental health › Bipolar Disorder and Treatment
- Keywords
- GABAergic interneurons, dorsolateral prefrontal cortex, major depressive disorder, bipolar disorder, mood disorders, somatostatin, parvalbumin, calretinin, glutamic acid decarboxylase, GAD65, GAD67, gene expression, age-related decline
- MeSH terms
- Adult, Age Factors, Aged, Bipolar Disorder, Female, gamma-Aminobutyric Acid, Humans, Male, Middle Aged, Nerve Tissue Proteins, Neurons, Parvalbumins, Protein Precursors, RNA, Messenger, Somatostatin, Biomarkers, Down-Regulation, Prefrontal Cortex, Mood Disorders, Reverse Transcriptase Polymerase Chain Reaction
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