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.