Objective: To analyze changes in morphological characteristics of rat frontal cortex neurons during myocardial ischemia. Methodology: Experiments were performed on 12 male non-pedigreed white rats with an initial weight of 240±20 g. Myocardial ischemia in white mongrel rats was modeled by isoprenaline administration. The material was sampled 24 hours after the last injection of the drug. Results: Experimental myocardial ischemia was accompanied by a slight decrease in neuronal size and pericarion deformation. The number of hyperchromic wrinkled neurons increased. Wrinkled neurons constituted the majority of cells in the studied cortex section. Conclusion: During experimental myocardial ischemia, parietal cortex neurons decreased in size by 3.3% compared to control (p<0.05), the shape of neurons slightly changed - they became more elongated (by 6.4%) (p<0.05), while the form factor decreased by 5.5% (p<0.05) compared to control. The number of normochromic neurons decreased by 8% (p<0.05), while the number of hyperchromic neurons increased 2-fold compared to controls. Hyperchromic shriveled neurons appeared, their number amounted to 4.5% of the number of all neurons.

The role of neuroglobin in ischemia has not been studied in detail. A number of studies indicate its neuroprotective effect, other data refute its importance for the survival of neurons in conditions of lack of oxygen. In the course of the conducted studies, the neuroprotective role of neurooglobin in certain types of cerebral ischemia has been established. The results obtained resolve the contradiction noted in the literature data about the role of neuroglobin in the pathogenesis of cerebral ischemia and show that in certain models of cerebral ischemia, with sufficient time to implement compensatory mechanisms, neuroglobin participates in neuroprotection, while in forms of cerebral ischemia, where this time is insufficient, its content decreases and there is no neuroprotective effect.

Aim . To study the morphology of neurons in the cerebral cortex of rat pups on day 20 under conditions of administration of a nitric oxide synthase inhibitor (NOS) during placentation. Materials and methods . Outbred white female rats (n = 12) were randomly divided into 2 groups of 6 rats each. On the 11th day of pregnancy, the experimental group received a single intramuscular injection of N(omega)-nitro-L-arginine methyl ester (L NAME) at a dose of 25 mg/kg, in the control group – once intramuscularly 0.9% NaCl solution. Born rat pups were randomly selected one from the mother. On the 20th day, after medical euthanasia, the brain was collected. In the anterior part of the frontal cortex, we studied the density and area of neurons, the size and shape of perikarya and the severity of their staining with toluidine blue. Results . In the experimental group of 20-day-old rat pups, compared to the control group, the density and area of neurons were less by 10% (p > 0.05) and 22% (p > 0.05), respectively, the shape of the perikarya also changed to elongated, the elongation factor increased by 0.3 units. (p < 0.05) and there was a sixfold increase in the proportion of hyperchromic neurons (p < 0.05), hyperchromic wrinkled (p < 0.001) neurons appeared, which were absent in control animals. Conclusion. Morphological changes in neurons of the cerebral cortex in rat pups born from females who received a NOS inhibitor during placentation may be a consequence of a decrease in the formation of nitric oxide in the neurons themselves and in the endothelium of the vessels supplying the brain

Neuroglobin (Ngb) is a member of the globin family. Like other globin proteins, it is involved in the maintenance of oxygen homeostasis. Ngb distribution in the normal brain is well known, but its response to pathological injury, such as cerebral ischemia, has not yet been adequately elucidated. One primary reason for this is that ischemic lesions in cerebral tissues have mostly been studied in transgenic organisms. In addition, the available data on Ngb content are limited to a small number of brain structures. This article examines the patterns of changes in Ngb immunoreactivity in neurons from different parts of the rat brain after subtotal cerebral ischemia of varying duration. An immunohistochemical study of Ngb content in 25 brain structures of white male Wistar rats exposed to 30-min and 3-h subtotal cerebral ischemia was performed. A decrease in Ngb content in all structures (especially 3 h after the ischemia onset and in the phylogenetically older parts), temporal mediation, and dependence on the phylogenetic age were revealed. The obtained results further decipher the correlation between the changes in Ngb content and the degree of cerebral ischemic damage, which is necessary to clarify the functions of the studied protein.

A mediator is a physiologically active substance found in a nerve cell in a bound form, which is secreted from an excited nerve ending into the synaptic cleft and specifically acts on the receptors of the postsynaptic target cell. When a neurological stimulus reaches the end of a nerve fiber, neurotransmitters are produced, and by diffusing across the synapse, they cause the impulse to be transferred to another nerve fiber, a muscle fiber, or some other component. CNS comprises neurotransmitter indicators in the form of genes and proteins that are expressed uniquely in various cells. The major neurotransmitter indicators’ neurological, developmental, and pathological functions are demonstrated in this article.

Acute cerebrovascular accident is one of the most urgent problems in modern medicine. The urgency of the problem of cerebrovascular diseases can rightfully be defined as extraordinary, requiring the concentration of efforts of specialists of different profiles to solve it. One of the promising neuroprotective amino acids is L-arginine. Most of the effects caused by this amino acid are associated with its ability to increase the formation of NO, acting as a source for its formation. It has been shown that the use of L-arginine reduces the size of the infarct, reduces vascular tone and causes a hypotensive effect, prevents and corrects ischemic and reperfusion damage to the brain and other organs. The use of "L-arginine" in animals of the group with cerebral ischemia and the introduction of a non-selective NOS inhibitor – L-NAME did not have a significant positive effect. Thus, nitric oxide hyperproduction has been studied by stimulating synthesis by introducing the substrate L-arginine, and inhibition by using the non-selective NO synthase inhibitor N-nitro-L-arginine methyl ester.

Introduction. ATP synthase is a key component of ATP synthesis. The study of its content in brain neurons in experimental cerebral ischemia may reflect changes in the functional state of different neurons and their sensitivity to the pathological effect. The study aimed to reveal patterns in ATP synthase immunoreactivity in neurons of various parts of the rat brain during subtotal ischemia of various durations. Materials and methods. Modeling of subtotal cerebral ischemia (SCI) was carried out by ligation of both common carotid arteries (n=12: control group – n=4, 30-minute SCI – n=4, 3-hour SCI – n=4); the control animals underwent a sham surgery. Frontal paraffin sections were stained according to the Nissl method to identify brain structures and immunohistochemically for ATP synthase. ATP synthase immunoreactivity was expressed in units of optical density ×103. Results. Changes in the immunoreactivity of ATP synthase in brain structures occur to varying degrees and not in all studied structures. The most pronounced and rapid decrease in the content of ATP synthase was observed in telencephalon, namely in the temporal and retrosplenial agranular cortex. The least pronounced changes in the cortex were in the structures of the hippocampus, in the neurons of layer II of the CA2 field. In the structures of the thalamus, hypothalamus, and midbrain the dynamic varied. In the structures of the medulla oblongata, the decrease in immunoreactivity occurs more slowly and less pronounced. Conclusion. During experimental cerebral ischemia the degree and rate of change in the content of ATP synthase in rat brain structures vary greatly and depend both on the brain region and the neurotransmitter nature of neurons. Keywords: ATP synthase, ischemia, immunohistochemistry, brain, rat

The study of the brain in health and disease is a relevant and promising area of modern science and, in this regard, a frequent topic of dissertation research. Cerebral ischemia leads to a number of general and local metabolic and functional disorders, the pathogenesis of which is complex, many-sided and largely unclear. The absence of pronounced morphological changes in the simulation of PCI after 1 hour in rats is explained by the compensation of blood circulation in the circle of Willis.

Introduction. The role of neuroglobin ischemia is still unclear. Some studies indicate its neuroprotective effect due to increased expression of endothelial NOS. Other evidence refutes its significance for neuronal survival under oxygen-deficient conditions, as neuroglobin deficiency appears to increase HIF-1α expression. Materials and methods. The experiments were performed on 56 male outbred white rats weighing 258±18 g. Total cerebral ischemia was simulated by decapitation of animals, whereas the subtotal one was simulated by simultaneous ligation of both carotid arteries. Stepwise subtotal cerebral ischemia was performed by ligating both carotid arteries with an interval of 7 days (subgroup 1), 3 days (subgroup 2), or 1 day (subgroup 3). Results. The study found significant differences in neuroglobin content across three subgroups. In subgroup 1, there was a notable increase in neuroglobin content compared to the control group, with a 13% increase in the parietal cortex (p<0.05) and a 14% increase in the hippocampus (p<0.05). However, subgroup 2 showed a decrease in neuroglobin content, with a 13% decrease in the parietal cortex (p<0.05) and a 7% decrease in the hippocampus (p<0.05). The most significant decrease in neuroglobin content was observed in subgroup 3, with a 31% decrease (p<0.05) in the parietal cortex and a 33% decrease (p<0.05) in the hippocampus. In subgroup 3, the parietal cortex showed a 40% decrease in neuroglobin content compared to subgroup 1 (p<0.05) and a 21% decrease compared to subgroup 2 (p<0.05). Similarly, the hippocampus exhibited a 42.6% decrease in neuroglobin content compared to subgroup 1 (p<0.05) and a 28% decrease compared to subgroup 2 (p<0.05). Conclusion. Thus, the most pronounced disorders of the prooxidant-oxidant balance decreased neuroglobin were observed during a 1-day total cerebral ischemia. Keywords: neuroglobin, ischemia, pyramidal neurons, hippocampus, parietal cortex

Introduction . Amino acids and their derivatives are involved in synaptic transmission as neurotransmitters and neuromodulators, and some of them are involved in the formation of neurotransmitters of the nervous system. Therefore, the study of the state of the amino acid pool in incomplete cerebral ischemia plays a significant role. The objective was to assess the nature of changes in amino acid pool and evaluate their participation in oxidative processes in rats with incomplete cerebral ischemia. Methods and materials . The experiments were carried out on 16 male outbred white rats weighing 260±20 g in compliance with the requirements of the Directive of the European Parliament and of the Council No. 2010/63/EU of September 22, 2010 on the protection of animals used for scientific purposes. Results. Compared with the indicators in the control group, rats with an ischemic period of 1 hour in the parietal lobe had a decrease in the content of sulfur-containing amino acids: methionine by 12 % and cysteate by 28 %. In addition, there was an increase of L-arginine in the parietal lobe by 39 %, and in the hippocampus – by 56 %. Conclusions . The following changes are characteristic for one-hour incomplete cerebral ischemia: a decrease in the content of sulfur-containing amino acids, with a decrease in both methionine and an increase in the content of L-arginine. Changes in the parietal lobe and hippocampus had a similar nature, except for the absence of a drop in the level of cysteate in the hippocampus, as a reflection of the higher sensitivity of the parietal lobe to oxygen deficiency, compared with the hippocampus.

Biogenic amines play an important role in brain metabolism and functioning, participation in synaptic transmission as neurotransmitters and neuromodulators (dopamine, serotonin, histamine and others). Catecholamines are formed from the essential amino acid phenylalanine by hydroxylating it to tyrosine with the enzyme phenylalanine-4-hydroxylase, which is subsequently converted to dioxyphenylalanine (DOPA) with tyrosine-3-hydroxylase.

Cerebrovascular diseases of ischemic genesis tend to increase, rejuvenate, are associated with severe clinical course, high rates of disability and mortality. The urgency of the problem of cerebrovascular diseases can rightfully be defined as extraordinary, requiring the concentration of efforts of specialists of different profiles to solve it. Subtotal cerebral ischemia leads to the development of morpho functional disturbances of the cerebral cortex. The introduction of Omega-3 polyunsaturated fatty acids has a corrective effect on the hippocampus in conditions of subtotal ischemia, reducing the number of shadow cells and hyperchromic shrunken neurons, without significantly affecting the size and shape of neurons in the cerebral cortex. Prior administration of L-NAME, the use of Omega-3 did not prevent the effects of the NO synthase inhibitor and associated NO deficiency at this dose and route of administration.

The aim of this study was to elucidate the ultrastructure of neurons in the parietal cortex and hippocampus of rats with subtotal cerebral ischemia against the background of the introduction of omega-3 polyunsaturated fatty acids.The neurons of the hippocampus, as a phylogenetically older part of the cerebral cortex, are less sensitive to hypoxia, which may be the reason for the therapeutic effect of Omega3 polyunsaturated fatty acids.Thus, the administration of ω-3 polyunsaturated fatty acids has a corrective effect on the ultrastructure of hippocampal neurons under conditions of subtotal cerebral ischemia, which manifested itself in an increase in the density of mitochondrial cristae and a decrease in the density of lysosomes.

Results: Dystrophic changes constitute an extensive group of neuronal disorders and are manifested at the morphological level by deformation of the perikarions and neuropil, wrinkling or swelling of the cell, and changes in the chromatophilia of the cytoplasm. At the electron microscopic level, disorganization of organelles is observed, reflecting gross violations of the vital processes of the neuron. There are several ways to regenerate neurons: intracellular regeneration, restoration of the neuropil, the formation of new neurons (in some parts of the nervous system - the hippocampus, the subventricular layer of the lateral ventricles and olfactory bulbs) and the formation of heterokaryons (fusion of a neuron with an oligodendrocyte). Hypertrophy of neurons may indicate both compensation and the development of a pathological process. To clarify the nature of this phenomenon, it is necessary to conduct an ultramicroscopic study of the organelles of the nerve cell.

I Ion channels are complex protein structures comprising the molecular systems of opening, closing, selectivity, inactivation and regulation. This review article aims to generalize and systematize literature data on the structural and functional characteristics of ion channels and methods for investigating their activity. Violations of the activity of ion channels may alter the functioning of both individual cells and the entire organism. Therefore, further research into the structural and physiological characteristics of ion channels can be considered promising and relevant.

Objective. To analyze the changes in the size and shape of perikaryons and the degree of cytoplasm chromatophilia of the rat hippocampal and parietal cortex neurons at different periods after the modeling of total cerebral ischemia. Material and Methods. The experiments were performed on 42 male outbred white rats with an initial weight of 240 ± 20 g. Total cerebral ischemia in white outbred rats was modeled by decapitation. The material for further histological examination was taken at the 1st, 5th, 15th, 30th and 60th minutes, as well as 5 and 24 hours after decapitation. The study of histological preparations was carried out using an Axioscop 2 plus microscope, a digital video camera and the ImageWarp image analysis program. Among the total number, the cells were isolated by the intensity of cytoplasm staining (chromatophilia). After a preliminary check for the normal distribution of indicators, the data obtained were analyzed by non-parametric statistics. Results. With total cerebral ischemia, a decrease in the size of neurons and deformation of perikaryons were observed. Normochromic neurons completely disappeared at the 60th minute. The number of hyperchromic neurons increased, and then progressively decreased. Shrunken neurons made up the majority of cells in the studied cortical sections at the 30–60th minutes, and then, after 5 and 24 hours, cells with pericellular edema prevailed in the neuron population.Conclusion. The obtained data on histological changes in neurons of phylogenetically different parts of the cerebral cortex in the dynamics of total cerebral ischemia provide the basis for further detailed study of post-mortem changes of the brain as well as determining the time of death, thus creating a fundamental basis for studying the properties of neurons, including their transition from one functional state to another.

Objective. To analyze the changes in the size and shape of perikaryons and the degree of cytoplasm chromatophilia of the rat hippocampal and parietal cortex neurons at different periods after the modeling of total cerebral ischemia. Material and Methods. The experiments were performed on 42 male outbred white rats with an initial weight of 240 ± 20 g. Total cerebral ischemia in white outbred rats was modeled by decapitation. The material for further histological examination was taken at the 1st, 5th, 15th, 30th and 60th minutes, as well as 5 and 24 hours after decapitation. The study of histological preparations was carried out using an Axioscop 2 plus microscope, a digital video camera and the ImageWarp image analysis program. Among the total number, the cells were isolated by the intensity of cytoplasm staining (chromatophilia). After a preliminary check for the normal distribution of indicators, the data obtained were analyzed by non-parametric statistics. Results. With total cerebral ischemia, a decrease in the size of neurons and deformation of perikaryons were observed. Normochromic neurons completely disappeared at the 60th minute. The number of hyperchromic neurons increased, and then progressively decreased. Shrunken neurons made up the majority of cells in the studied cortical sections at the 30–60th minutes, and then, after 5 and 24 hours, cells with pericellular edema prevailed in the neuron population.Conclusion. The obtained data on histological changes in neurons of phylogenetically different parts of the cerebral cortex in the dynamics of total cerebral ischemia provide the basis for further detailed study of post-mortem changes of the brain as well as determining the time of death, thus creating a fundamental basis for studying the properties of neurons, including their transition from one functional state to another.