Guest editorial
The GABA System in Schizophrenia: Cells, Molecules and Microcircuitry

https://doi.org/10.1016/j.schres.2015.07.017Get rights and content

Abstract

This is an overview of several papers that have been published in the Special Issue of Schizophrenia Research entitled The GABA System in Schizophrenia: Cells, Molecules and Microcircuitry. This issue presents a broad range of original reports and scholarly reviews regarding recent progress in studies of neural circuitry in corticolimbic brain regions in patients with schizophrenia.

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Role of funding source

No funding for this Guest Editorial.

Contributors

No other contributors for this Guest Editorial but all the authors of the articles in this Special Issue contributed to its development.

Conflict of interest

Dr. Benes has no COIs of any kind.

Acknowledgment

This overview describes several studies that have been funded by the National Institutes of Health and other private organizations. For details, refer to the Acknowledgments in the individual papers.

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Cited by (35)

  • The Role of the GABAergic System in Diseases of the Central Nervous System

    2021, Neuroscience
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    Beneyto and colleagues showed that in Schizophrenia mice, the mRNA expressions of α1 and α5 subunits of the GABAA receptors were decreased, while α2 subunit was increased and there was no change in α3 subunit (Beneyto et al., 2011). Another research added that the GABAA receptors are up-regulated in Schizophrenia (Benes, 2015). Additionally, the levels of the α2 subunit of the GABAA receptors on the axon initial segment of pyramidal neurons were increased in subjects with Schizophrenia (Volk et al., 2001).

  • Salience network glutamate and brain connectivity in medication-naïve first episode patients – A multimodal magnetic resonance spectroscopy and resting state functional connectivity MRI study

    2021, NeuroImage: Clinical
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    This might pinpoint to a biological mechanism where higher concentration of glutamate is related to stronger SN FC/dopamine activity in HC, and this particular mechanism might be impaired in FEP. Finally, postmortem studies of the dACC in schizophrenia have reported both GABA-ergic interneurons alterations (Benes, 2015), as well as decrease in the number of both excitatory and inhibitory synapses (Roberts et al., 2020). Those findings are consistent with recent large scale genome wide association (GWAS) studies in schizophrenia that identified variations in genes involved in synaptic function and neuronal signaling, including those associated with glutamatergic function (Marshall et al., 2017; Schizophrenia Working Group of the Psychiatric Genomics, 2014), as well as with the findings that common-variants identified by those GWAS map to a limited set of neurons, including pyramidal cells and interneurons (Skene et al., 2018).

  • Amelioration of cognitive impairments induced by GABA hypofunction in the male rat prefrontal cortex by direct and indirect dopamine D<inf>1</inf> agonists SKF-81297 and D-Govadine

    2020, Neuropharmacology
    Citation Excerpt :

    Thus, pharmacotherapeutics that target impairments in working memory and other aspects of cognition associated with these disorders may significantly improve psychiatric outcomes. In schizophrenia, deficits in PFC GABA function have been posited as a potential pathophysiological mechanism underlying cognitive impairment (Benes, 2015; Tse et al., 2015). Decreased protein and mRNA expression of the GABA synthesis enzyme GAD67 have consistently been observed in PFC from schizophrenia patients (Curley et al., 2011; Akbarian et al., 1995), in conjunction with changes in other markers of PFC GABA function (Beasley et al., 2002).

  • SNAP-25 in Major Psychiatric Disorders: A Review

    2019, Neuroscience
    Citation Excerpt :

    Clinical presentation of SZ is varied but must include a prominent thought disorder or hallucinations (APA, 2013). While the pathology of SZ is still largely unknown, research to understand its biology suggests it is a neurodevelopmental disorder involving several different areas of neuropathology, including synaptic functioning and neural plasticity (Benes, 2015; Jouroukhin et al., 2016). Studies using animal models of SZ, human postmortem tissue, and human genetics have called attention to the possible involvement of SNAP-25.

  • Influence of Venus and Mars in the cognitive sky of schizophrenia. Results from the first-step national FACE-SZ cohort

    2018, Schizophrenia Research
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    Oestrogen is a significant modulator of gut permeability and the microbiome (Diebel et al., 2015) and therefore may have indirect effects on how the immune system shapes brain development. More direct effects on brain immunity may also be relevant, with sex differences evident in the colonization and function of central nervous system microglia, with consequences for central development (Schwarz et al., 2012) Neuroanatomical data indicates an array of sex differences in central changes, including SZ men showing: greater ventricular enlargement, a higher number of cerebral abnormalities (Nopoulos et al., 1997), and a reversal of the normal left-greater-than-right male asymmetry in the inferior parietal lobule (Frederikse et al., 2000) as well as sex differences in the expression of GABAergic genes in the anterior cingulate cortex in SZ (Benes, 2015; Bristow et al., 2015). Cognitive symptoms can have a higher impact on the outcome, and quality of life, of SZ than any other symptom (Shin et al., 2016), and are considered a core feature of this disorder (Elvevåg and Goldberg, 2000).

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