Mitochondrial dynamics significantly play a major role in the pathogenesis of neurodegenerative diseases, such as Parkinson’s disease and Alzheimer’s disease. The dysregulation of mitochondrial biogenesis and function, characterized by impaired fission and fusion processes mediated by a number of proteins, in particular, Drp1, Mfn1, Mfn2, Opa1, and PGC-1α, contributes to neuronal vulnerability and degeneration. Insufficient mitophagy and disrupted mitochondrial transport exacerbate oxidative stress and neurotoxicity. Emerging therapeutic strategies that target mitochondrial dynamics, including various pharmacological agents, demonstrate potential for restoring mitochondrial balance and enhancing neuroprotection. This growing body of research underscores the importance of mitochondrial health in developing effective interventions for neurodegenerative conditions. This review highlights well-established links between the disruption of mitochondrial dynamics and the development of neurodegenerative processes. We also discuss different therapeutic strategies that target mitochondrial function in neurons that have been proposed as perspective neuroprotective treatments.

The review addresses current ideas about the morphological and histophysiological features of the brain capillary endothelium with a special focus on the ultrastructure of endotheliocytes, which are part of the neurovascular unit. The relationship between their main characteristics and the implementation of the barrier function is discussed. The specificity of intercellular contacts in capillary endotheliocytes within the blood–brain barrier (BBB) and the structure of their cytoskeleton and glycocalyx are analyzed. The structural peculiarities of capillaries in the neurogenic niches, as well as in the anatomical formations, where the BBB is absent or poorly expressed, are considered. A separate section of the review is devoted to transcellular transport of substances (transcytosis) in cerebral endotheliocytes. Despite a wealth of publications on the subject, many issues remain unresolved, and the study of the structure and functioning of the cerebral microvascular endothelium is still on the agenda.

Transcranial magnetic stimulation (TMS) is a non-invasive method for targeted modulation of the electrical activity of brain neurons with a magnetic field. Although TMS efficacy was demonstrated in the treatment of several neurological and mental disorders, changes in nervous tissue at the cellular and molecular levels with different duration and intensity of stimulation have been relatively understudied by cellular neurobiology methods. Aim. The aim of this review was to evaluate and summarize new experimental data on the fundamental mechanisms underlying the action of TMS and its potential in modulating structural and functional changes in nervous tissue. This article summarizes recent data on the effects of different TMS protocols on the mechanisms underlying synaptic plasticity, neurogenesis, and neuronal differentiation. Separate sections summarize the neuroprotective effects of this method and glial microenvironment response. Studies to investigate the mechanisms of TMS will contribute to the development of more effective and reliable treatment protocols.

In recent years, the dynamics of mitochondrial transformations in cells have been of more concern to both representatives of basic science and researchers in the field of applied medicine. A growing number of observations demonstrate the important regulatory influence of mitochondrial dynamics on a variety of physiological and pathological processes in many, if not all, organ and tissue structures. The prospects for studying the features and regulators of these processes for understanding the pathogenesis of diseases, developing their new biomarkers, as well as treatment technologies seem increasingly significant.   The purpose of this article is to review the facts obtained regarding mitochondrial dynamics, which, from the authors’ point of view, deserve the attention of pediatricians. The volume of relevant information turned out to be too extensive to fit into one article, which forced it to be divided into several successive publications. The first part provides information about the main processes included in the concept of “mitochondrial dynamics,” the importance of maintaining the balance of the latter for ontogenesis and tissue homeostasis, as well as data on its disturbances in diseases of the nervous system in children.

The following review considers current concepts concerning the characteristics of DRP1-related mitochondrial division in brain cells during hypoxic-ischemic pathology. The functional role of DRP1 in neurons and astroglia in cerebral ischemia conditions was analyzed. We discuss the potential for regulating DRP1 activity through the selective inhibitor of mitochondrial fission, mdivi-1. The article also presents data on DRP1 involvement in astro- and microglia-mediated intercellular mitochondrial transport. Understanding of the molecular mechanisms responsible for mitochondrial fission during hypoxic-ischemic exposure will allow us to consider DRP1 as an effective therapeutic target for treating conditions with a hypoxic component.

Introduction. Astrocytes are involved in mediator metabolism, neuroplasticity, energy support of neurons and neuroinflammation, and this determines their pathogenetic role in epilepsy. Aim. This study aimed at evaluating region-specific changes in the distribution of functional astroglial proteins in reactive astrocytes in a kainate-induced model of mesial temporal lobe epilepsy. Materials and methods. The localization and expression of functional astroglial proteins (i.e. aquaporin-4, connexin-43, EAAT1/2, and glutamine synthetase) in the hippocampus CA3 region, dentate gyrus, and stratum lucidum layer were evaluated by immunofluorescence 28 days after intra-hippocampal administration of kainic acid to animals. Results. Changes were heterogeneous in different hyppocampus subregions. Astrocytes of the stratum lucidum associated with mossy fibers showed the highest vulnerability and decreased content and/or disturbed localization of the channels and transporters that form membrane complexes in the processes. Disturbances in homeostatic functions of astrocytes aggravated the adverse processes both on the side where the toxin was injected and in the contralateral hippocampus.