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The Role of Neuroglia in the Development and Progression of Schizophrenia.
Biomolecules
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.
View Article and Find Full Text PDFGenetic and Neurochemical Profiles Underlying Cortical Morphometric Vulnerability to Parkinson's Disease.
Brain Res Bull
January 2025
Department of Radiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. Electronic address:
Background: Increasing evidence has documented cortical involvement at all stages of PD. The local vulnerabilities within certain brain regions in PD have been previously demonstrated, whereas its underlying genetic and neurochemical factors remain unclear. This study aims to investigate the spatial spectrum of cortical atrophy in Parkinson's disease (PD) and link these variances in gray matter properties and curvature respectively to putative molecular pathways and neurotransmitter factors.
View Article and Find Full Text PDFExploring Serotonin-1A receptor function in the effects of buspirone on cognition by molecular receptor expression and EEG analytical studies.
Eur J Pharmacol
January 2025
Dr. Panjwani Center for Molecular Medicine and Drug Research, International Center for Chemical and Biological Sciences, University of Karachi, Karachi, 75270, Pakistan.
Buspirone, a commonly prescribed medication for generalized anxiety disorder (GAD), is gaining attention for its narrow window of side effects such as lack of physical dependence, non-sedative properties as compared to other anxiolytic drugs. Its dose-specific therapeutic effects beyond anxiety highlights its clinical significance. Pharmacologically, buspirone activates serotonin-1A pre-synaptic autoreceptors and post-synaptic heteroreceptors which modulate serotonergic neurotransmission induced behavioral changes such as anxiolytic and nootropic effects.
View Article and Find Full Text PDFMolecular Mechanisms of Nicergoline from Ergot Fungus in Blocking Human 5-HT3A Receptor.
J Microbiol Biotechnol
November 2024
Department of Biotechnology and Department of Integrative Food, Bioscience and Biotechnology (BK21 FOUR), Chonnam National University, Gwangju 61186, Republic of Korea.
This study investigates the modulatory effects of nicergoline, a major bioactive compound derived from ergot fungus, on the 5-hydroxytryptamine 3A (5-HT3A) receptor. Utilizing a two-electrode voltage-clamp technique, we evaluated the impact of nicergoline on the 5-HT-induced inward current (I) in 5-HT3A receptors. Our findings reveal that nicergoline inhibits I in a reversible and concentration-dependent manner.
View Article and Find Full Text PDFBlockade of mGluR1 and mGluR5 in the lateral habenula produces the opposite effects in the regulation of depressive-like behaviors in the hemiparkinsonian rats.
Exp Neurol
January 2025
Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Xi'an 710061, China. Electronic address:
Depression is one of the most common non-motor symptoms in Parkinson's disease (PD) and the hyperactivity of the lateral habenula (LHb) may contribute to depression. The present study was performed to investigate the effects and mechanisms of group I metabotropic glutamate receptors (mGluRs) in the LHb on PD-related depressive-like behaviors. Unilateral 6-hydroxydopamine lesions of the substantia nigra pars compacta (SNc) were used to establish the PD rat model.
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