ArticleBiological psychiatry2025
Alterations in Prefrontal Cortical Somatostatin Neurons in Schizophrenia: Evidence for Weaker Inhibition of Pyramidal Neuron Dendrites.
Article in Biological psychiatry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Apical integration theory provides a neural basis for understanding disorganization and consciousness in the schizophrenias.Current research in neurobiology · 2026Article
- Environmental enrichment modulates parvalbumin interneuron deficits and plasticity-related signaling after early postnatal NMDA receptor hypofunction in male rat visual cortex.Brain structure & function · 2026Article
- Transcriptional Profiles of Somatostatin and Parvalbumin Interneuron Subtypes in the Human Dorsolateral Prefrontal Cortex: Implications for Schizophrenia.The American journal of psychiatry · 2026Article
- Uncovering the signatures of aging and senescence in the human dorsolateral prefrontal cortex.Cell genomics · 2026Article
- Cell Density and mRNA Expression of Inhibitory Interneurons in Schizophrenia: A Meta-Analysis.bioRxiv : the preprint server for biology · 2025Article
- Common Genomic and Proteomic Alterations Related to Disturbed Neural Oscillatory Activity in Schizophrenia.International journal of molecular sciences · 2025Review
- Brain-derived neurotrophic factor prevents LPS-induced dysregulation of GABAergic interneuron markers in mouse hippocampus.Frontiers in cellular neuroscience · 2025Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
backgroundCertain cognitive processes require inhibition provided by the somatostatin (SST) class of GABA (gamma-aminobutyric acid) neurons in the dorsolateral prefrontal cortex (DLPFC). This inhibition onto pyramidal neuron dendrites depends on both SST and GABA signaling. Although SST messenger RNA (mRNA) levels are lower in the DLPFC in schizophrenia, it is not known whether SST neurons exhibit alterations in the capacity to synthesize GABA, principally via the 67-kilodalton isoform of glutamic acid decarboxylase (GAD67).
methodsGAD67 and SST mRNA levels were quantified in individual SST neurons using fluorescence in situ hybridization in DLPFC layers 2/superficial 3, where SST neurons are enriched, in individuals with schizophrenia (n = 46) and unaffected comparison (n = 46) individuals. Findings were compared with GAD67 and SST mRNA levels quantified by polymerase chain reaction and to final educational attainment, a proxy measure for cognitive functioning.
resultsGAD67 (F
conclusionsDeficits in both GAD67 and SST mRNAs within SST neurons indicate that these neurons have a markedly reduced ability to inhibit postsynaptic pyramidal neuron dendrites in schizophrenia. These alterations likely contribute to cognitive dysfunction in schizophrenia.
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