Increased [3H]kainic acid binding in the prefrontal cortex in schizophrenia☆
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2022, Nanocarriers for Drug-Targeting Brain TumorsA comparative analysis of kainate receptor GluK2 and GluK5 knockout mice in a pure genetic background
2021, Behavioural Brain ResearchCitation Excerpt :KARs have been linked to psychiatric disorders such as schizophrenia, bipolar disorder, major depressive disorder, and autism [2,8]. In an early pharmacological study, [3H]kainic acid binding sites were measured in the post-mortem brains of schizophrenia patients, and a 25–50 % increase in [3H]kainic acid binding was observed in the medial frontal regions and the areas responsible for eye-movement [9]. The expression of mRNA in KAR subunits is also reduced in the orbitofrontal cortex of patients with schizophrenia [10–12].
Positive allosteric modulators of metabotropic glutamate 2 receptors in schizophrenia treatment
2015, Trends in NeurosciencesCitation Excerpt :Recent findings suggest that the mGlu2Rs are also expressed postsynaptically, where they play a key role in the control of the responses induced by atypical antipsychotics [28–31]. Additional evidence for involvement of glutamate in the pathophysiology of schizophrenia comes from postmortem studies which revealed altered ionotropic glutamate receptor binding and gene expression mainly in the prefrontal cortex and the hippocampus [32–35]. Furthermore, functional neuroimaging studies have shown reduced NMDA binding in the hippocampus of medication-free schizophrenic patients compared to healthy controls [36].
Clozapine and GABA transmission in schizophrenia disease models: Establishing principles to guide treatments
2015, Pharmacology and TherapeuticsCitation Excerpt :A reduction in PFC glutamate transmission is also posited to contribute at least in part to cortical hypofrontality as evidenced by post-mortem reports of decreased PFC glutamate levels in schizophrenia (Tsai et al., 1995). In this regard, an increase in PFC glutamate receptor density as evidenced by increased 3H-kainate binding (Nishikawa et al., 1983) and NMDAR 2D subunit mRNA expression (Akbarian et al., 1996) have been reported in schizophrenia. In addition, a 23% reduction in dlPFC pyramidal neuron dendritic spine number has also been reported in schizophrenia which is suggested to reflect reduced thalamocortical and/or corticocortical afferent input (Glantz & Lewis, 2000).
Abnormal N-linked glycosylation of cortical AMPA receptor subunits in schizophrenia
2013, Schizophrenia ResearchTargeting glutamate system for novel antipsychotic approaches: Relevance for residual psychotic symptoms and treatment resistant schizophrenia
2012, European Journal of Pharmacology
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Supported by Grant 81-13-07 (1981) from National Center for Nervous, Mental and Muscular Disorders of the Ministry of Health and Welfare, Japan.
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We thank Drs. T. Kanaya, M. Naito, H. Yamazumi, T. Koizumi, H. Nomura, T. Fujimori, O. Matsuda, S. Ando, S. Takahashi, H. Shimada, H. Morioka, T. Numakura and J. Semba for their help in obtaining specimens. We also thank Drs. K. Kishi, T. Maeda, A. Sakuma, B. Scatton and S. Watanabe for their helpful advice. We are grateful tto Dr. T. Inose for his histopathological examination of the brain of case S3.