Postmortem studies, using various methods and directed at several molecular targets, have provided increasing evidence that glutamatergic neurotransmission is affected in schizophrenia. The bulk of the data are in the hippocampus, wherein there is reduced expression of one or more subunits for all three ionotropic receptors (NMDA, AMPA, and kainate). Presynaptic glutamatergic markers, notably the vesicular glutamate transporter VGLUT1, may also be decreased in schizophrenia, especially in older subjects. CA1 appears less affected than other subfields, and the decrements may be greater in the left than in the right hippocampus. The recently described susceptibility genes for schizophrenia all act upon glutamatergic synaptic transmission, which may, therefore, be part of the core pathophysiology of the disorder.
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http://dx.doi.org/10.1196/annals.1300.006 | DOI Listing |
Int J Mol Sci
January 2025
National Cancer Institute, P. Baublio Str. 3B, LT-08406 Vilnius, Lithuania.
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January 2025
Azriele Faculty of Medicine in the Galilee, Bar-Ilan University, Safed 1311502, Israel.
Provoked vulvodynia (PV) is the leading cause of vulvar pain and dyspareunia. The etiology of PV is multifactorial and remains poorly understood. PV is associated with a history of repeated vulvar inflammation and is often accompanied by sensory neuromodulation as a result of activation of the metabotropic glutamate receptor 5 (mGluR5) in the sensory nerve terminals.
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January 2025
Department of Pathology, Faculty of Health Care and Social Work, Trnava University and University Hospital, 917 02 Trnava, Slovakia.
The autoantibodies against the NR1 subunit are well known in the pathomechanism of NMDAR encephalitis. The dysfunction of the NR2 subunit could be a critical factor in this neurological disorder due to its important role in the postsynaptic pathways that direct synaptic plasticity. We report a case of paraneoplastic anti-NMDAR encephalitis presented alongside very severe illness.
View Article and Find Full Text PDFBiomolecules
January 2025
Department of Neurology, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China.
Reactive astrogliosis and acidosis, common features of epileptogenic lesions, express a high level of astrocytic acid-sensing ion channel-1a (ASIC1a), a proton-gated cation channel and key mediator of responses to neuronal injury. This study investigates the role of astrocytic ASIC1a in cognitive impairment following epilepsy. Status epilepticus (SE) in C57/BL6 mice was induced using lithium-pilocarpine; the impact of ASIC1a on astrocytes was assessed using rAAV-ASIC1a-NC and rAAV-ASIC1a-shRNA, injected in the CA3 region of mice.
View Article and Find Full Text PDFBiomolecules
December 2024
Neurochemical Research Unit and Bebensee Schizophrenia Research Unit, Department of Psychiatry and Neuroscience and Mental Health Institute, University of Alberta, Edmonton, AB T6G 2G3, Canada.
Schizophrenia is a complex heterogenous disorder thought to be caused by interactions between genetic and environmental factors. The theories developed to explain the etiology of schizophrenia have focused largely on the dysfunction of neurotransmitters such as dopamine, serotonin and glutamate with their receptors, although research in the past several decades has indicated strongly that other factors are also involved and that the role of neuroglial cells in psychotic disorders including schizophrenia should be given more attention. Although glia were originally thought to be present in the brain only to support neurons in a physical, metabolic and nutritional capacity, it has become apparent that these cells have a variety of important physiological roles and that abnormalities in their function may make significant contributions to the symptoms of schizophrenia.
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