Showing papers by "Natalia V. Gulyaeva published in 2020"
TL;DR: Epileptiform activity is frequent in the acute period of TBI period and is associated with distant hippocampal damage on a microscopic level, and the FPI model is suitable for exploring pathogenetic mechanisms of post-traumatic disorders.
Abstract: Background: In humans, early pathological activity on invasive electrocorticograms (ECoGs) and its putative association with pathomorphology in the early period of traumatic brain injury (TBI) remains obscure. Methods: We assessed pathological activity on scalp electroencephalograms (EEGs) and ECoGs in patients with acute TBI, early electrophysiological changes after lateral fluid percussion brain injury (FPI), and electrophysiological correlates of hippocampal damage (microgliosis and neuronal loss), a week after TBI in rats. Results: Epileptiform activity on ECoGs was evident in 86% of patients during the acute period of TBI, ECoGs being more sensitive to epileptiform and periodic discharges. A “brush-like” ECoG pattern superimposed over rhythmic delta activity and periodic discharge was described for the first time in acute TBI. In rats, FPI increased high-amplitude spike incidence in the neocortex and, most expressed, in the ipsilateral hippocampus, induced hippocampal microgliosis and neuronal loss, ipsilateral dentate gyrus being most vulnerable, a week after TBI. Epileptiform spike incidence correlated with microglial cell density and neuronal loss in the ipsilateral hippocampus. Conclusion: Epileptiform activity is frequent in the acute period of TBI period and is associated with distant hippocampal damage on a microscopic level. This damage is probably involved in late consequences of TBI. The FPI model is suitable for exploring pathogenetic mechanisms of post-traumatic disorders.
11 citations
TL;DR: The results lead to the conclusion that the contribution of hyperlocomotion must be taken into account in the interpretation of behavioral measures in the elevated plus maze test.
Abstract: Removal of the olfactory bulbs induces a multitude of behavioral impairments, the most reproducible of which is hyperlocomotion. Olfactory bulbectomy is widely used to model anxiety and depression-like states. In the present study, C57Bl/6 mice subjected to olfactory bulbectomy were tested in standard tests to assess anxiety and depression-like behavior. Removal of the olfactory bulbs in mice was found to increase anxiety and emotionality. Attention in the present work was focused on the fact that hyperactivity induced by bulbectomy can seriously distort the results obtained in anxiety tests. The results lead to the conclusion that the contribution of hyperlocomotion must be taken into account in the interpretation of behavioral measures in the elevated plus maze test.
4 citations
TL;DR: The increase in the level ofCNTF in lacrimal fluid of patients with depression indirectly indicates an increase in CNTF in the aqueous humor of the anterior chamber of the eye, and possibly in the cerebrospinal fluid, which, requires further study.
Abstract: —We studied the content of brain-derived neurotrophic factor (BDNF) and ciliary neurotrophic factor (CNTF) in serum and lacrimal fluid in 105 patients with depression (unipolar depression, 37 and bipolar depression, 68). The stimulated lacrimal fluid was taken from one randomly selected eye with a pipette dispenser. The concentrations of BDNF and CNTF were determined by enzyme-linked immunosorbent assay. We observed a decrease in the concentration of BDNF in the blood serum of patients (22 380 ± 3600 pg/mL) compared to healthy controls (25 220 ± 3550 pg/mL). The concentration of CNTF in patients was increased both in blood serum (6.7 ± 2.8 compared with 4.4 ± 2.3 pg/mL) and in lacrimal fluid (35.8 ± 9.8 vs 31.0 ± 5.3 pg/mL). CNTF values in blood serum and in the lacrimal fluid weakly correlated with each other. The increase in the level of CNTF in lacrimal fluid of patients with depression indirectly indicates an increase in CNTF in the aqueous humor of the anterior chamber of the eye, and possibly in the cerebrospinal fluid, which, requires further study.
3 citations
TL;DR: The data indicate that 1.5 months after the administration of immunotoxin, microglia are activated only in the neocortical areas, not in the striatum or olfactory bulbs.
Abstract: —The immunotoxin 192IgG-saporin is a powerful tool for inducing the selective death of cholinergic neurons in the basal nuclei. In this study, we investigated the effect of intracerebroventricular immunotoxin administration on the state of microglia in tissues adjacent to the ventricle (striatum and parietal cortex) and remotely located but receiving innervation from the medial septal region and diagonal band of Broca (entorhinal cortex and olfactory bulbs). Assessment of the state of glial cells was performed using immunohistochemical staining with antibodies against the microglial marker protein IBA-1 and against the astrocytic marker protein GFAP. It turned out that, in the parietal cortex, the number of microglial cells increased, however this increase was not accompanied by changes in the state of astrocytes, while in the striatum there were no changes in the state of glial cells. Analysis of the expression of the Ncf1 and Cx3Cr1 genes showed that the expression of Ncf1 increases in both the parietal and entorhinal cortex in the absence of changes in the expression of Cx3Cr1. In the striatum and olfactory bulbs, there were no changes in the expression of these genes. We also analyzed mRNA levels of the Ptprb and Slc22a8 genes expressed in blood vessels. Decreased Slc22a8 expression was observed only in the striatum, while the expression of the Ptprb gene did not change in any of the structures. The data indicate that 1.5 months after the administration of immunotoxin, microglia are activated only in the neocortical areas, not in the striatum or olfactory bulbs.
3 citations
TL;DR: In this paper, a review focusing on studies of pain threshold and tolerance in individuals with nonsuicidal self-injurious (NSSI) behavior is presented, with issues in animal modeling of NSSI discussed separately.
Abstract: This review focuses on studies of pain threshold and tolerance in individuals with nonsuicidal self-injurious (NSSI) behavior. The data on methods of pain sensitivity studies are presented, with issues in animal modeling of NSSI discussed separately. The results of neuroimaging studies on pain sensitivity in individuals with NSSI are described, along with contribution of genetic factors, psychological variables, and disturbances in opioid and hypothalamic-pituitary-adrenal systems. A critical methodological analysis of the studies on pain sensitivity in individuals with NSSI was performed.
1 citations
TL;DR: In this paper, a review analyzes data on biomarkers shared by stroke, depression, and post-stroke depression, showing that some overlap with stroke and depression, however, some differences are also present (IFN-γ, serum ferritin, VEGF, serotonin, dopamine, and miRNA expression).
Abstract: —Post-stroke depression (PD) is a complex multifactorial disease that affects over 30% of stroke survivors. Despite the high prevalence of the disease, important aspects of its classification, etiology, and pathogenesis are still not fully understood, which is complicated even further by significant difficulties in diagnostics and prevention. Subjective depression rating scales and physical examination as primary methods for diagnosis of post-stroke depression strongly depend on the doctor. The use of specific biomarkers may be effective, however, their identification, validation, and introduction to everyday practice continues to be a challenge. It is still not known whether potential biomarkers for post-stroke depression are a combination of depression and stroke markers, or whether they bear a certain specificity. The current review analyzes data on biomarkers shared by stroke, depression, and post-stroke depression. A number of PD biomarkers overlap with stroke and depression markers, however, some differences are also present (IFN-γ, serum ferritin, VEGF, serotonin, dopamine, and miRNA expression). On the other hand, stroke has an impact on the expression of depression markers. To identify biomarkers specific for post-stroke depression, further extensive studies are necessary.
1 citations
TL;DR: Contrary to the assumption, HuD-BDNF 3′-UTR interaction and BDNF expression in the frontal cortex differentially change in a manner dependent on the context of morphine action.
Abstract: Brain-derived neurotrophic factor (BDNF) mediates opiate dependence phenomenon. In the brain of morphine dependent animals BDNF level is controlled transcriptionally, however, post-transcriptional ...
1 citations
TL;DR: This review considers several mechanisms linked in particular with the functions of the transmitter systems and the neurotrophin, cytokine, and glucocorticoid systems, which determine maturation of intercellular communications in the hippocampus on the background of neuroinflammation and the sequelae of impairments to this process.
Abstract: Neuroinflammatory processes, particularly those induced by infectious agents, are associated with activation of the microglia and subsequent increases in the secretion of proinflammatory cytokines. Proinflammatory stimuli acting in early postnatal ontogeny are stress factors and, along with neuroinflammation, trigger the mechanisms of the stress response. If the proinflammatory signal is sufficiently powerful, the response to it can lead to modification of the body’s stress resistance and an increase in the risk of developing psychopathology accompanied by cognitive impairments at later stages of ontogeny, including in adults. This review considers several mechanisms linked in particular with the functions of the transmitter systems and the neurotrophin, cytokine, and glucocorticoid systems, which determine maturation of intercellular communications in the hippocampus on the background of neuroinflammation and the sequelae of impairments to this process.
1 citations
TL;DR: This study is the first to use the “unfolded maps” approach for detailed analysis of damage to the functional zones of the neocortex in the acute period of TBI.
Abstract: Objectives. Establishment of a link between the nature of damage to the neocortex and the functional manifestations of this damage is important for understanding the mechanisms of development of acute convulsions and their sequelae. Analysis of immediate convulsions in patients with traumatic brain injury (TBI) in practice is extremely difficult but can be performed in animal models. Study aims. To compare damage to functional areas in the neocortex with the semiology of immediate convulsive seizures and behavioral impairments in the acute period after TBI. Materials and methods. Studies were carried out using 48 Wistar rats. TBI was modeled by application of lateral hydrodynamic blows to the area of the right sensorimotor cortex. Video recordings were made at the moment of trauma and for 5 min into the post-trauma period, which provided for studies of the semiology of convulsive seizures. This was followed by use of a series of tests assessing the animals’ behavior. Results and conclusions. This study is the first to use the “unfolded maps” approach for detailed analysis of damage to the functional zones of the neocortex in the acute period of TBI. The focus of damage in the cortex increased over 3–7 days and was complex in shape, far removed from the limits of the area of direct action. Blows induced immediate convulsions, whose variability could not be explained only by the involvement of defined areas of the neocortex, along with behavioral impairments which could be the manifestations of developing necrosis largely in the sensory areas of the neocortex.