Sensomotor Cortex Research Articles

The role of ВK<sub>Са</sub> and IK<sub>Са</sub> channels in H<sub>2</sub>S-induced dilatation of pial arteries in rats after nephrectomy

BACKGROUND. Chronic kidney disease (CKD) is accompanied by the development of endothelial dysfunction, leading to a decrease in arterial reactivity to vasoactive agents. Uremia causes a change in the dilatation of arteries in various vascular regions, incl. and arteries of the pial membrane of the brain. The action of hydrogen sulfide (H2S), which can induce relaxation of smooth muscle cells of blood vessels, is currently considered a possible route of vasoprotection in various diseases, particularly, in CKD. THE AIM. To evaluate the role of calcium-activated potassium channels of large (BKCa) and intermediate (IKCa) conductance in H2S-induced dilatation of pial arteries in nephrectomized (NE) rats. MATERIAL AND METHODS. In Wistar rats nephrectomy (NE) was performed by resection of 5/6 of the renal tissue mass. Sham-operated (LO) animals served as control. The reaction of the pial arteries of the sensomotor cortex of NE and control SO rats to the application of H2S under physiological conditions and against the background of the use of BKCa channel blockers – tetraethylammonium (TEA) and IKCa – channels – TRAM-34. RESULTS. 4 months after NE, the application of H2S led to the dilatation of a smaller number of pial arteries (1.4 – 1.7 times) compared with SO rats. The preliminary exposure to TEA led to a decrease in the number of pial arteries responding by dilatation to the action of H2S in NE and SO rats. Against the background of the action of TRAM-34, the number of dilated arteries decreased under the action of H2S in SO rats, while in NE rats it practically did not change. CONCLUSION. Under physiological conditions, dilatation of the pial arteries in rats under the action of H2S is realized (at least in part) through the activation of the BKCa and IKCa channels of the membrane of endothelial and smooth muscle cells. Uremia, caused by nephrectomy, leads to impairment of the mechanism of dilatation of pial arteries, mediated by activation of calcium-activated potassium channels intermediate conductance apparently due to dysfunction of endothelial cells.

The Involvement of Insulin-Like Growth Factor 1 and Nerve Growth Factor in Alzheimer's Disease-Like Pathology and Survival Role of the Mix of Embryonic Proteoglycans: Electrophysiological Fingerprint, Structural Changes and Regulatory Effects on Neurotrophins.

Alzheimer’s disease (AD)-associated neurodegeneration is triggered by different fragments of amyloid beta (Aβ). Among them, Aβ (25–35) fragment plays a critical role in the development of neurodegeneration—it reduces synaptic integrity by disruption of excitatory/inhibitory ratio across networks and alters the growth factors synthesis. Thus, in this study, we aimed to identify the involvement of neurotrophic factors—the insulin-like growth factor 1 (IGF-1) and nerve growth factor (NGF)—of AD-like neurodegeneration induced by Aβ (25–35). Taking into account our previous findings on the neuroprotective effects of the mix of proteoglycans of embryonic genesis (PEG), it was suggested to test its regulatory effect on IGF-1 and NGF levels. To evaluate the progress of neurodegeneration, in vivo electrophysiological investigation of synaptic activity disruption of the entorhinal cortex–hippocampus circuit at AD was performed and the potential recovery effects of PEG with relative structural changes were provided. To reveal the direct effects of PEG on brain functional activity, the electrophysiological pattern of the single cells from nucleus supraopticus, sensomotor cortex and hippocampus after acute injection of PEG was examined. Our results demonstrated that after i.c.v. injection of Aβ (25–35), the level of NGF decreased in cerebral cortex and hypothalamus, and, in contrast, increased in hippocampus, prompting its multidirectional role in case of brain damage. The concentration of IGF-1 significantly increased in all investigated brain structures. The administration of PEG balanced the growth factor levels accompanied by substantial restoration of neural tissue architecture and synaptic activity. Acute injection of PEG activated the hypothalamic nucleus supraopticus and hippocampal neurons. IGF-1 and NGF levels were found to be elevated in animals receiving PEG in an absence of amyloid exposure. We suggest that IGF-1 and NGF play a critical role in the development of AD. At the same time, it becomes clear that the neuroprotective effects of PEG are likely mediated via the regulation of neurotrophins.

Oxygen Regime and Exchange of Ammonia in the Sensomotor Cortex of Cats During Blood Loss and Hyperbaric Oxygenation

Purpose.To study the effect of hyperbaric oxygenation (HBO) on the oxygen regime and ammonia metabolism in the neurons of cat cortex in hemorrhagic shock.Material and methods.Experiments were performed on 164 cats (males). The effect of HBO (3 ATA, 50 min) on cerebral blood flow (CBF), oxygen tension (PO2), the content of ammonia (Am), glutamine (Gn), glutamate (Gt), α-ketglutarate (α-KG), the activity of glutamate dehydrogenase (GDG), glutamine synthetase (GS), phosphate-dependent glutaminase (PDG) activity was studied in the sensorimotor cortex (SMC); the content of Am, GN and oxygen parameters in arterial (AB) blood and venous blood (VB) of the sagittal sinus in hemorrhagic shock caused by fractional bloodletting of their femoral artery at a rate of 10ml/kg/10 min in an average volume of 24±0.8 ml/kg, which was stopped with a decrease in systolic blood pressure to the level of 60.0±1.5 mm Hg. HBO was commenced on post-hemorrhagic minute 10 following the regimen of 3 ATA for 60 min.Results.The decrease in CBF and PO2in SMC develops as early as the 10th minute of hemorrhagic shock, progressing to the stage of hemorrhagic shock decompensation (60±14 min). Accumulation of Am in the SMC at the stage of hemorrhagic shock decompensation associated with stimulation of PDG and GDG activity, inhibition of hemorrhagic shock activity and deficiency of α-KG. HBO, without eliminating hypoxia in SMC, prevented the development of the decompensation stage in animals with GS, pathological accumulation of Am, and a decrease in the activity of hemorrhagic shock. HBO increases the Gn increment from the SMC, into the blood. Under HBO conditions, the stimulating effect of hypoxia on GDG activity remains, but the concentration of glutamate remains within the normal range, as does the activity of PDG.Conclusion.Hyperbaric oxygenation, without eliminating hypoxia in SMC, which develops in hemorrhagic shock, prevents a violation of the exchange of ammonia in it, caused by acute non-compensated blood loss.

Пластичность нейронов сенсомоторной коры в условиях повышенного радиационного фона

Purpose: Observe the changes in the structural and functional organization of the sensomotor cortex neurons throughout the post-radiation period. Material and methods: White male rats (120 animals) were irradiated on the “Hizatron» γ-rays 60Co single dose of 0.5 Gy with a dose rate of 0.5 Gy/h. Material taken away by 100 min; 5 hr; 1, 3, 7 and 14 days, 1, 6, 12 and 18 months after irradiation. Counted the number of neurons with different tinctorial properties, was calculated the nerve cell index, morphometric characteristics of nerve cells and content of nucleic acids. The obtained data were statistically processed, followed by mathematical modeling. Results: By the end of the post-radiation period the number of normochromic neurons decreased due to increasing the number of hyper- and hypochromic cells, as well as their destructive forms. In animals as the control and exposed groups values nerve-cell index decrease with age. In control and exposed groups of rats values nerve-cell index decrease with age. The dynamics of the cytoplasm shows a negative correlation with an index of the contents of cytoplasmic RNA. By the end of the experiment the content of RNA in the cytoplasm of neurons corresponded to the age control. Profile index of nuclear DNA in all periods of post-radiation is negatively correlated with cross-sectional area of the nuclei. The amplitude of fluctuations in the size of nucleoli of neurons was significantly greater than the corresponding figure in the cytoplasm and nuclei. In the period from 6 to 18 months post-radiation period RNA content in the nucleolus had a positive correlation with the index size. Immediately after the exposure indicator nucleocytoplasmic index exceeded the reference values, subsequently decreased, and by the end of postradiation period – almost matched up to it. Nucleolus-nuclear index immediately after irradiation not changed, in subsequent periods had a phase-change, but at 18 months matched to age-control. Conclusion: Research has shown that neuromorphological effects were nonlinear stochastic nature, and exposure to these parameters had no significant effect on neurons. However, some indicators are not always consistent with the age-control, which could affect their functional activity.

The effect of vascular peptide bioregulator on microcirculation in the brain cortex of old rats

Using a TV device to study brain microcirculation, we found that after a course of vascular peptide bioregulator the density of microvascular network of pia matter of old rats (22-24 months) sensomotor cortex increased about 2,5-2,8 times compared to control old rates; and noradrenaline-induced constriction reactions and acetylcholine-induced dilative reactions of the pial arterioles increased significantly. This perfusion in the tissue of the cerebral cortex is not increased, but the degree of blood oxygen saturation in the microvasculature of this tissue region raised.

Gender Differences in Postresuscitative Brain Structural Changes

Objective: to reveal gender differences in brain structural changes after clinical death and to assess the neuroprotective properties of the hormonal agent Gynodian Depot. Materials and methods. The brain neuronal populations were morphometrical-ly studied in adult albino rats of both sexes which had sustained 10-minute cardiac arrest. At minute 30 after resuscitation, oil solution of estradiol with dehydroepiandrosterone was intramuscularly injected into the study group animals in doses of 0.1 and 5 mg/100 g. The comparison group of animals received the equivalent volumes of saline. Gender- and age-matched intact rats served as a control. An image analysis system of cresyl violet-stained paraffin brain sections was used to determine the density and composition of highly ischemia-perfusion-sensitive populations of pyramidal neurons of Layer V of the sensomo-tor cortex, the CA1 and CA4 hippocampal sectors, and Purkinje cells in the lateral cerebellum. Results. It has been established that there are gender differences in brain morphology in health, which are detectable in the postresuscitative period. The site of lesions has been found to be different in resuscitated rats of different gender. At the same time, male brain lesions are more extensive, i.e. these involve to this or that extent all the examined regions: the cerebellum and CA4 hippocamplal sector exhibit neuronal death; the cortex and CA1 hippocampal sector show dystrophic changes in the nerve cells. In the females, neuronal shedding processes were observed in the CA1 hippocampal sector only. Estradiol + dehydroepiandrosterone treatment has been ascertained to prevent nerve cell death only in the males and to fail to affect the density and composition of the neuronal populations under study in the females. Conclusion. The findings suggest that it is important to identify the structural bases of sexual dimorphism in the body’s reaction to ischemic exposure and that it is necessary to take them into account when developing effective therapy and choosing the optimal treatment policy to correct posthypoxic encephalopathies. Key words: gender differences, postresuscitative neuronal changes, hormonal therapy, morphometry.

Significance of Immunohistochemical Studies of Heat Shock Proteins of the HSP70 Family in the Investigation of Postresuscitative Brain Changes

Objective: to evaluate the immunological responsiveness of various neuronal populations of heat shock proteins of the HSP 70 family and to reveal their association with the magnitude of postresuscitative neuronal morphological changes. Materials and methods. The hypoxia-highly sensitive neuronal populations of pyramidal neurons in the layer of the fifth cerebral sensomotor cortex and hippocampal sectors CA1 and CA4 throughout the postresuscitative period after 12-minute cardiac arrest were subject to a complex immunocytochemical and morphometric study. Their immunological responsiveness to the thermal shock proteins was determined by the indirect peroxidase-antiperoxidase test using the polyclonal antibodies to HSP70. The density and composition of neuronal populations were ascertained by the morphometric assay. Results. The baseline immunological responsiveness of neuronal populations has been demonstrated to be an important factor of its resistance to ischemic lesions. The authors have determined a trend in postresuscitative changes in the immunological responsiveness of neuronal populations to HSP70 and established its association with the development of nerve cell dystrophic changes. They discuss whether complex immunocytochemical and morphometric studies are promising in investigating the mechanisms of postresuscitative brain abnormality. Conclusion. By and large, the findings suggest that the role of HSP70 in maintaining the homeostasis of neuronal populations is more complex and multifactorial, as earlier considered, and it is unlikely to be restricted itself to only merely neuroprotective properties. The high baseline content of HSP70 makes a considerable contribution to the resistance of neuronal populations to ischemia-reperfusion; and the changes in the immunological responsiveness to HSP70 are closely associated with the development of pathological nerve cell changes during a postresuscitative process.

Effect of ionizing radiation on the protein-synthesizing system of brain neurons of ground squirrels in different functional states

Using fluorescence and electron microscopy, it is shown that the physiological state of ground squirrels exposed to ionizing radiation at different stages of the torpor-awakeness (hypothermia-normothermia) cycle is the main factor responsible for changes in the protein-synthesizing system of neurons in the hippocampus (fields CA1 and CA3) and the sensomotor cortex. The neurons of animals irradiated in the state of awakeness are less radioresistant and recover more slowly than neurons of animals irradiated in torpor, with the difference being more distinct in neurons of the CA1 field. The effect of irradiation is weak in animals entering torpor and reaches a peak in awakening animals. It is proposed that the inhibition of protein synthesis in the latter case takes place at the elongation stage, with heavy polysomes formed in the cytoplasm of neurons.

553 Reorganization of somatosensory afferent projections after injury of the senso-motor cortex in men

The potential for reorganization in the adult brain has been largely underestimated in the past and we are just beginning to understand the organisational principles involved in functional recovery. A bulk of experimental evidences have been accumulated in support of the hypothesis that neuronal aggregates adjacent to a lesion in the cortical brain areas can be progressively vicarious to the function of the damaged neurones. Such a reorganisation, if occurring in the affected hemisphere of a patient with a monohemispheric lesion, should significantly modify the interhemispheric symmetry of somatotopic organisation of the sensorimotor cortices, both in terms of absolute surfaces and number of “recruited” neurons, as well as of spatial coordinates. In fact, a roughly symmetrical organisation of sensorimotor — particularly for the hand contorl — in the right and left hemisphere has been observed in healthy humans by different methods of functional brain imaging, including fMRI, TMS, MEG, HD-EEG. Not uniform results about the functional brain activity related to sensory, motor and cognitive functions in normal and diseased subjects are often due to differences in the experimental paradigm designed as well as in the spatial and temporal resolution of the neuroimaging techniques used. The multi-modal integration of data obtained with several neuroimaging techniques allowed a coherent modelling of human brain higher functions. Functional magnetic resonance imaging (fMRI) provided fine spatial details (millimetres) of the brain responses, which were compared with the cortical maps of the motor output to different body districts obtained with transcranial magnetic stimulation (TMS). Magnetoencephalography (MEG) ability to study sensorimotor areas by analysing cortical magnetic fields, is also complementary to the motor cortex topographical mapping provided by TMS. MEG high temporal resolution allows to detect relatively restricted functional neuronal pools activated during cerebral processing of external stimuli. Moreover, these brain responses can be investigated with magnetoencephalography (MEG) and high density electroencephalography (EEG) techniques, with elevated time resolution (ms). With respect to the high resolution EEG technique, the MEG technique allowed a more precise localisation of the sites of neural activity buried into the cortical sulci, but was unable to detect the response of the crown of the cortical giri and of the frontal-mesial cortex (including the supplementary motor area), because of its poor sensitivity to radially oriented dipoles. The integration of functional and anatomical information provide cues on the relationship between brain activity and anatomic sites where this takes place, allowing the characterisation of the physiological activity of the cortical brain layers as well as to study the plastic reorganisation of the brain in different pathological conditions following stroke, limb amputation, spinal cord injury, hemisperectomy.

Morphochemical changes in brain structures in the course of chronic haloperidol treatment and the correction of these changes with tuftsin.

The systemic injection of haloperidol (4 wk, 0.5 mg/kg/d) caused the increase of protein concentration and content, and the activity level of aminopeptidase in the cytoplasm of the neurons of associated type (layer III). The nucleus of these cells decreased both in sizes and in the content of proteins. In the neurons of efferent-projectory type (layer V), the decrease of studied peculiarities as compared with control level was observed. Tuftsin (300 micrograms/kg/d) injection after chronic haloperidol treatment causes the restoring action on changed parameters in sensomotor cortex. In caudate nucleus, tuftsin influence caused further reduction of neuron's cytoplasmic area and significant reduction in protein content. The received results testify to the morphobiochemical heterogenity of investigated brain structures, which is displayed both in the case of haloperidol treatment and in the case of its correction by neuropeptide tuftsin. Chronic haloperidol administration to animals can develop a model of certain symptoms and syndromes of parkinsonism. Its most pronounced manifestation is an imbalance in the neuromediator systems, especially the dopaminergic one (Mettler and Crandall, 1959; Colls, 1984; Funk et al., 1986). The research was performed in conjunction with the physiologists, whose experiments have shown that after chronic haloperidol administration, changes in animal behavior are developed that are typical for bradikinesia, and the motor regimen of integration is disturbed (Popova and Kachalova, 1991; Dovedova and Povova, 1993). Regulatory drugs, especially the tetrapeptide tuftsin, seem to correct such disturbances.

Effect of early cortical lesion on the acute model of epilepsy

The experiments were performed in order to investigate the sparing of function following early postnatal cortical lesion in the acute rat model of epilepsy. Sensomotor cortex was unilaterally removed at 9 and 10 days of postnatal age in lesioned animals, while control animals were only sham operated (at the same early stage of life) or non-operated (before implantation of the electrodes). Seizure activity was recorded by means of electroencephalograms at adult stage of life induced by parenteral administration of penicillin (1 000 000 I.U./kg, i.p.). Our results showed that when the cortical lesion was performed in infancy (on the contrary to the lesion performed in adulthood) there was no prolongation of seizure activity in an acute model of epilepsy.

Muscarinic cholinergic receptors of rat lymphocytes: effect of antigen stimulation and local brain lesion.

Expression of muscarinic cholinergic receptors (m-AchR) on thymocytes and lymphocytes supports a hypothesis of direct interaction between autonomic innervation and the immune system. Using a muscarinic antagonist, [3H]quinuclidinyl benzilate ([3H]QNB), we revealed different characteristics of m-AchR expression in lymphocytes isolated from the spleen, peripheral blood or thymus of Wistar rats. To further explore the mechanisms controlling m-AchR expression in lymphocytes we have addressed two questions: (i) whether local brain lesions will affect [3H]QNB binding activity of lymphocytes and (ii) whether different antigens will alter m-AchR expression in lymphocytes. We report here that electrolytic lesions of the area hypothalamica anterior resulted in a significant increase in [3H]QNB-specific binding in thymocytes 7 days after neurosurgery. In contrast, local lesions of other hypothalamic structures (area preoptica medialis, area hypothalamica posterior) or sensomotor cortex did not affect m-AchR expression in thymocytes. No apparent changes of [3H]QNB-binding activity were found in lymphocytes isolated from rat spleen or peripheral blood after operation. Both T-cell-dependent (sheep red blood cells) and T-cell-independent (Vi antigen of Salmonella typhi) antigens induced a significant increase in [3H]QNB-specific binding in spleen lymphocytes while [3H]QNB-binding activity of peripheral blood lymphocytes did not change. A different pattern of lymphocyte m-AchR expression found in various lymphoid tissues after immunization or brain lesions suggests a local involvement of cholinergic mechanisms in neuroimmune interaction.

Effect of leucine-enkephalin on after-discharge development in the rat sensomotor cortex

Effect of leucine-enkephalin on after-discharge development in the rat sensomotor cortex

Reparative changes in the sensomotor cortex of the offspring after moderate prenatal exposure to alcohol

Reparative changes in the sensomotor cortex of the offspring after moderate prenatal exposure to alcohol

Biogenic amines in brain structures of rats of different zoosocial rank during immobilization stress

The content of monoamines and their metabolites in different parts of the brain: mesencephalic reticular formation, locus coeruleus, sensomotor cortex was studied by high-performance liquid chromatography in rats with different zoo-social position. Content of dopamine and serotonin in the brain structures studied was found to be different in dominants and subdominants. Maximal changes of monoamines under immobilization stress were observed in dominants.

Relations between the superior colliculus and sensomotor cortex in conscious rabbits

The tonic influence of the superior colliculus (SC) on the formation of visual evoked responses of the sensomotor cortex (SMC) was demonstrated in experiments on conscious rabbits. The influence of SC on the function of SMC was found to be realized with the involvement of tectothalamocortical (through the nucleus lateral is posterior thalami — NLPT) connections. SMC of the conscious rabbit, in turn, exerts a phasic inhibitory influence on visual function of SC. The findings are discussed in the light of involvement of tectocortical and corticotectal inter-relations in the organization of visuomotor integration, which is essential for visually controlled behavior.

State of the dendritic spines of pyramidal neurons in layer V of the rat sensomotor cortex after 14-day space flight

State of the dendritic spines of pyramidal neurons in layer V of the rat sensomotor cortex after 14-day space flight

Changes in parameters of the after-discharge in the rat sensomotor cortex after cessation of conditioning repetitive electrical stimulation

Changes in parameters of the after-discharge in the rat sensomotor cortex after cessation of conditioning repetitive electrical stimulation

Microvesicles in developing synapses

The sensomotor cortex and nucleus caudatus of the embryonal (14-22 days) and newborn rats have been investigated by electron microscopic method. There were described two groups of microvesicles (10-20 nm in diameter) with smooth and rough external surface. They differ from other vesicular components of the developing synapses (such as synaptic vesicles, vesicles of growing conus and other) by the minimal size, structure and localization. Microvesicles with the rough external surface are found only at that moment when the membranous specialization of the further synapse from desmosomes begins to form. They are found along the membranes of active contact zone and are correlated with the degree of differentiation of these membranes. Microvesicles with the smooth external surface are found during the all period of synaptogenesis. They are found either in presynaptic terminal freely or they are attached to presynaptic membrane where they form cluster of microvesicles and they can be found on the surface of synaptical vesicles too. In this article the functional role and genesis of microvesicles are discussed.

Character of formation of a generator of pathologically enhanced excitation (epileptic focus) in the rat sensomotor cortex during repetitive electrical stimulation

Character of formation of a generator of pathologically enhanced excitation (epileptic focus) in the rat sensomotor cortex during repetitive electrical stimulation