Abstract
Here, we show that volume neurotransmission and the redox property of dopamine, as well as redox-regulated processes at glutamate receptors, can contribute significantly to our understanding of schizophrenia. Namely, volume neurotransmission may play a key role in the development of dysconnectivity between brain regions in schizophrenic patients, which can cause abnormal modulation of NMDA-dependent synaptic plasticity and produce local paroxysms in deafferented neural areas. During synaptic transmission, neuroredox regulations have fundamental functions, which involve the excellent antioxidant properties and nonsynaptic neurotransmission of dopamine. It is possible that the effect of redox-linked volume neurotransmission (diffusion) of dopamine is not as exact as communication by the classical synaptic mechanism, so approaching the study of complex schizophrenic mechanisms from this perspective may be beneficial. However, knowledge of redox signal processes, including the sources and molecular targets of reactive species, is essential for understanding the physiological and pathophysiological signal pathways in cells and the brain, as well as for pharmacological design of various types of new drugs.
Highlights
Converging evidence for the neurodevelopmental theory of schizophrenia suggests that a disturbance of brain development, involving genetic and environmental factors, during the intrauterine period and the first few years after birth underlies the later appearance of psychosis during adulthood [1]
Since metabotropic glutamate receptors (mGluRs) can modulate the release of dopamine, and act via protein kinases and cysteine protease (ROS play essential roles in regulating their enzymatic activity) signaling pathways that affect mitochondrial processes, indicating that mGluR associated signal pathways are redox-linked processes
Burke suggested [151] that schizophrenic visual hallucinations may be due to deafferentation and dysintegration of definite visual structures that induce an increase in the excitability of deafferented neurons
Summary
Converging evidence for the neurodevelopmental theory of schizophrenia suggests that a disturbance of brain development, involving genetic and environmental factors, during the intrauterine period and the first few years after birth underlies the later appearance of psychosis during adulthood [1]. Mitochondria take up about 25% of the cell volume in neurons and play fundamental roles in cellular redox and Ca2+ homeostasis, ATP generation, free radical production, regulation of neurotransmitter release, cell growth, apoptosis, cell signaling, iron metabolism, steroidogenesis, and many other functions [40, 58].
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
