Abstract— Numerous data obtained in the last 20 years indicate that all parts of the mature central nervous system, from the retina and olfactory bulb to the spinal cord and brain, contain cells connected by gap junctions (GJs). The morphological basis of the GJs is a group of joined membrane hemichannels called connexons, the subunit of each connexon is the protein connexin. In the central nervous system, connexins show specificity and certain types of them are expressed either in neurons or in glial cells. Connexins and GJs of neurons, combining certain types of inhibitory hippocampal and neocortical neuronal ensembles, provide synchronization of local impulse and rhythmic activity, thalamocortical conduction, control of excitatory connections, which reflects their important role in the processes of perception, concentration of attention and consolidation of memory, both on the cellular and at the system level. Connexins of glial cells are ubiquitously expressed in the brain, and the GJs formed by them provide molecular signaling and metabolic cooperation and play a certain role in the processes of neuronal migration during brain development, myelination, tissue homeostasis, and apoptosis. At the same time, mutations in the genes of glial connexins, as well as a deficiency of these proteins, are associated with such diseases as congenital neuropathies, hearing loss, skin diseases, and brain tumors. This review summarizes the existing data of numerous molecular, electrophysiological, pharmacological, and morphological studies aimed at progress in the study of the physiological and pathophysiological significance of glial and neuronal connexins and GJs for the central nervous system.

Cardiovascular, rheumatic, kidney, and neurodegenerative diseases and mental disorders are a common cause of deterioration in the quality of life up to severe disability and death worldwide. Many pathological conditions, including this group of diseases, are based on increased cell death through apoptosis. It is known that this process is associated with signaling pathways controlled by a group of gaseous signaling molecules called gasotransmitters. They are unique messengers that can control the process of apoptosis at different stages of its implementation. However, their role in the regulation of apoptotic signaling in these pathological conditions is often controversial and not completely clear. This review analyzes the role of nitric oxide (NO), carbon monoxide (CO), hydrogen sulfide (H2S), and sulfur dioxide (SO2) in apoptotic cell death in cardiovascular, rheumatic, kidney, and neurodegenerative diseases. The signaling processes involved in apoptosis in schizophrenia, bipolar, depressive, and anxiety disorders are also considered. The role of gasotransmitters in apoptosis in these diseases is largely determined by cell specificity and concentration. NO has the greatest dualism; scales are more prone to apoptosis. At the same time, CO, H2S, and SO2 are more involved in cytoprotective processes.

—As the population ages, age-related cognitive impairments are becoming an increasingly pressing problem. Currently, the role of polyamines (putrescine, spermidine, and spermine) in the pathogenesis of cognitive impairments of various origin is actively discussed. It was shown that the content of polyamines in the brain tissue decreases with age. Exogenous administration of polyamines makes it possible to avoid cognitive impairment and/or influence the pathogenetic processes associated with disease progression. There are 3 known ways that polyamines can enter the human body: food, synthesis by intestinal bacteria, and biosynthesis in the body. Currently, one of the most promising approaches to the prevention of cognitive impairment is the use of foods with a high content of polyamines, as well as the use of various probiotics that affect intestinal bacteria that synthesize polyamines. Since 2018, in a number of European countries projects have been launched aimed at evaluation of the impact of a diet high in polyamines on cognitive processes. The review, based on analysis of modern scientific literature and the authors' own data, presents material on the effect of polyamines on cognitive processes and the role of polyamines in the regulation of neurotransmitter processes, and discusses the role of polyamines in cognitive disorders in mental and neurological diseases.

Peripheral-nerve injury is a frequent cause of disability. Presently, no clinically effective neuroprotectors have been found. We have studied the NO-dependent expression of p53 in the neurons and glial cells of the dorsal root ganglia (DRG) of a rat’s spinal cord, as well as the role of NO in the death of these cells under the conditions of axonal stress, using sciatic-nerve axotomy as a model. It was found out that axotomy led to the nuclear–cytoplasmic redistribution of p53 in neurons, 24 h after trauma. The NO donor led to a considerable increase in the level of p53 in nuclei and, to a smaller degree, in the cytoplasm of neurons and karyoplasm of glial cells 4 and 24 h after axotomy. Application of a selective inhibitor of inducible NO-synthase (iNOS) provided the opposite effect. Introduction of the NO donor resulted in a significant increase in cell death in the injured ipsilateral DRG, 24 h and 7 days after trauma. The selective inhibitor of iNOS demonstrated a neuroprotective effect. Axotomy was shown to upregulate the iNOS in nuclei and cytoplasm of DRG cells. The NO-dependent expression of p53, which is particularly achieved through iNOS activation, is believed to be a putative signaling mechanism of neural and glial-cell death after axotomy.

AimThe aim of our studies was to discover responses of the membrane systems in neurons and cardiomyocytes as well as mechanisms of influences and effects produced by the broadband-spectrum stochastic electromagnetic radiation (BBSS EMR) on them according to data on membrane potential (MP) levels and action potential (AP) parameters obtained by us. Materials and methodsNeurons from the isolated central neural system (CNS) of the snail Helix pomatia were selected to serve as a model for our experiments. We applied an electrophysiological technique implying recording of intracellular potentials of a neuron. The presented research work is of fundamental nature and reveals some intimate mechanisms of actions made by electromagnetic radiation (EMR) on the cytoplasm membrane of a neuron and its channels that is applicable to cardiomyocytes. An absolutely exclusive distinctive feature of our work is that the specific BBSS EMR used in our experiments has unique characteristics and offers broadband stochastic radiated frequencies in the range from 10 n Hz to 10 m Hz at an integral radiation power of only 0,1 µW. Another distinguishing feature of the applied EMR parameters is that the stochastically organized EMR is supplied under such action rhythms, which are close to the natural alpha-, theta-and delta-rhythms of an EEG as well to the natural background base resonance frequency of the Earth, which has been physically measured to be 7,83 Hz, that is evolutionary significant for biological systems. Results and discussionWe are pioneers in the world science who succeeded in ob-