How do glial-neuronal interactions fit into current neurotransmitter hypotheses of schizophrenia?
Abstract
Evidence is accumulating that the exclusive dopamine hypothesis of schizophrenia has to be abandoned. Instead, a more integrative approach combines different neurotransmitter systems, in which glutamatergic, GABAergic and dopaminergic pathways interact. This paradigm shift coincides with the recognition that, while typical and modern atypical antipsychotic drugs have efficiently controlled the dramatic psychotic symptoms of schizophrenia, their impact on negative and cognitive symptoms is negligible. Indeed, cognitive decline is now believed to represent the core of schizophrenic morbidity and in this context, impairment of glutamate and more specifically NMDA function is of major importance. Given that astrocytes are important in controlling glutamate homeostasis, it is necessary to assign a significant role to glial-neuronal interactions in the pathophysiology of schizophrenia. Indeed, recent data from several animal and human studies corroborate this notion. This review outlines current neurotransmitter hypotheses and evidence for glial impairment in schizophrenia. Furthermore, findings from recent studies of (13)C nuclear magnetic resonance spectroscopy in experimental models of schizophrenia and NMDA hypofunction are presented and their implications for future research on glial-neuronal interactions discussed.
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Diminished glutamate receptor activation, in particular of the NMDA-type, may be a possible underlying mechanism of reduced synaptic activity because NMDA-receptor antagonists produce the same symptoms as those seen in schizophrenia.
“In fact, diminished glutamate receptor activation, in particular of the NMDA-type of glutamate receptor, may be a possible underlying mechanism of reduced synaptic activity because NMDA-receptor antagonists produce the same symptoms as those seen in schizophrenia.17,18,25”
From Glutamate in Schizophrenia: A Focused Review and Meta-Analysis of 1H-MRS Studies (2013) · cites this paper as [18]
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- Authors
- Kondziella, D., Brenner, E., Eyjolfsson, E. M., & Sonnewald, U.
- Affiliations
- Norwegian University of Science and Technology (NO)
- Corresponding author
- Sonnewald, Ursula
- Venue
- Neurochemistry International
- Publisher
- Elsevier BV
- Published
- 2007-01
- Volume
- 50
- Issue
- 2
- Pages
- 291-301
- ISSN
- 0197-0186 (ISSN-L)
- OpenAlex
- W2093539065
- Cited by
- 83
- References
- 74
- Citations by year
- 2025: 2 · 2024: 4 · 2023: 1 · 2021: 2 · 2020: 3 · 2019: 1 · 2018: 4 · 2017: 5 · 2016: 5 · 2015: 2 · 2014: 14 · 2013: 5 · 2012: 2
- FWCI
- 3.82
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neurochemistry International (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Amino Acid Enzymes and Metabolism
- Keywords
- schizophrenia, neuron-glia interactions, astrocytes, glutamate homeostasis, NMDA receptor hypofunction, glutamatergic neurotransmission, dopamine signaling, GABAergic neurotransmission, negative symptoms, cognitive symptoms, cognitive decline, atypical antipsychotics, schizophrenia pathophysiology
- MeSH terms
- Animals, Dopamine, Humans, Neuroglia, Neurons, Schizophrenia, Dizocilpine Maleate, Neurotransmitter Agents, Excitatory Amino Acid Antagonists, Glutamic Acid
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