RAS Pavlov Institute of Physiology

Saint Petersburg, Russia

RAS Pavlov Institute of Physiology

Saint Petersburg, Russia
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Dick O.E.,RAS Pavlov Institute of Physiology
Neurocomputing | Year: 2017

The task is to estimate quantitative features in involuntary oscillations of shaking (tremor) of fingers accompanied the performance of the motor task by healthy subjects, patients with Parkinson’ disease and individuals with the essential tremor. For solving the task the tremor patterns are examined by the wavelet-transform modulus maxima method and the recurrence quantification analysis. The physiological tremor is characterized by the minimal energy of the wavelet spectrum, the maximal degree of multifractality, the minimal degree of determinism and the maximal recurrence time density entropy, reflecting the greatest uncertainty of the period value. During the essential tremor the significant enhancement of the wavelet spectrum energy and the decrease of the dynamical complexity of involuntary oscillations are observed. It is evident as the fall in the multifractality degree, the growth of determinism in recurrence plots, the decrease of the recurrence time density entropy and the emergence of unstable periodic orbits in involuntary oscillations. For the parkinsonian tremor all the trends are enhanced that lead to more definite dynamics of patterns. Therefore, our results demonstrate that the dynamical complexity of patterns of involuntary oscillations decreases in larger degree for Parkinson’ disease, than for patients with the syndrome of the essential tremor, that is, it declines with increasing the severity degree of motor disorders. The results obtained for the first time can be applied for evaluating the degree of deviation of the motor function from the healthy one. © 2017

Rybnikova E.,RAS Pavlov Institute of Physiology | Samoilov M.,RAS Pavlov Institute of Physiology
Frontiers in Neuroscience | Year: 2015

Exposure of organisms to repetitive mild hypoxia results in development of brain hypoxic/ischemic tolerance and cross-tolerance to injurious factors of a psycho-emotional nature. Such preconditioning by mild hypobaric hypoxia functions as a "warning" signal which prepares an organism, and in particular the brain, to subsequent more harmful conditions. The endogenous defense processes which are mobilized by hypoxic preconditioning and result in development of brain tolerance are based on evolutionarily acquired gene-determined mechanisms of adaptation and neuroprotection. They involve an activation of intracellular cascades including kinases, transcription factors and changes in expression of multiple regulatory proteins in susceptible areas of the brain. On the other hand they lead to multilevel modifications of the hypothalamic-pituitary-adrenal endocrine axis regulating various functions in the organism. All these components are engaged sequentially in the initiation, induction and expression of hypoxia-induced tolerance. A special role belongs to the epigenetic regulation of gene expression, in particular of histone acetylation leading to changes in chromatin structure which ensure access of pro-adaptive transcription factors activated by preconditioning to the promoters of target genes. Mechanisms of another, relatively novel, neuroprotective phenomenon termed hypoxic postconditioning (an application of mild hypoxic episodes after severe insults) are still largely unknown but according to recent data they involve apoptosis-related proteins, hypoxia-inducible factor and neurotrophins. The fundamental data accumulated to date and discussed in this review open new avenues for elaboration of the effective therapeutic applications of hypoxic pre- and postconditioning. © 2015 Rybnikova and Samoilov.

Lyubashina O.A.,RAS Pavlov Institute of Physiology | Sokolov A.Y.,RAS Pavlov Institute of Physiology | Panteleev S.S.,RAS Pavlov Institute of Physiology
Neuroscience | Year: 2012

Vagus nerve stimulation (VNS) is an approved antiepileptic and antidepressant treatment, which has recently shown promise as a therapy for drug-resistant primary headaches. Specific neurobiological mechanisms underlying its anticephalgic action are not elucidated, partly because of the deficiency of research-related findings. The spinal trigeminal nucleus (STN) plays a prominent role in pathophysiology of headaches by modulating pain transmission from intracranial structures to higher centers of the brain. To determine whether vagal stimulation may affect trigeminovascular nociception, we investigated the effects of VNS on the STN neuronal activity in the animal model of headache. In anesthetized rats the spike activity of the STN neurons with convergent orofacial and meningeal inputs was monitored, and the changes in neuronal responses to electrical stimulation of the dura mater under preconditioning or under continuous electrical stimulation of the left cervical vagus nerve were studied. Preconditioning vagal afferent stimulation (200-ms train of pulses at 30 Hz applied before each dural stimulus) did not produce substantial changes in the STN spike activity. However, continuous VNS with frequency of 10. Hz in 48% of cases significantly suppressed trigeminal neuronal responses to dural electrical stimulation. In line with the decrease in evoked activity, the VNS-induced depression of ongoing neuronal firing was observed. Although the inhibitory effect was prevailing, 29.5% of STN neurons were facilitated by VNS, whereas 22.5% were unresponsive to the stimulation. These results provide an evidence of VNS-induced modulation of trigeminovascular nociception, and therefore contribute to a deeper understanding of neurophysiological mechanisms underlying effects of vagal stimulation in chronic drug-resistant headaches. © 2012 IBRO.

Filaretova L.,RAS Pavlov Institute of Physiology
Current Pharmaceutical Design | Year: 2013

Nonsteroidal anti-inflammatory drugs (NSAIDs) make significant contributions to gastric ulcer disease which remains widespread. Although several factors have been postulated as pathogenic elements of the gastric injury induced by NSAIDs, it is, however believed that prostaglandin deficiency plays a critical role in the pathogenesis of this injury. During prostaglandin deficiency, other defensive mechanisms might operate to attenuate NSAID-induced gastropathy. According to our results, NSAIDs, similar to stress, induce an increase in glucocorticoid production that in turn helps the gastric mucosa to resist the harmful actions of these drugs. In this article, we review our experimental data suggesting that glucocorticoids may play a role as natural defensive factors in maintaining the integrity of the gastric mucosa during NSAID therapy and might operate to attenuate NSAID-induced gastropathy. © 2013 Bentham Science Publishers.

Zolotarev V.A.,RAS Pavlov Institute of Physiology
Current Pharmaceutical Design | Year: 2014

In the stomach, pre-absorptive perception of food constituents is of particular importance in maintaining secretion and motility that matches the quantity and quality of nutrients. Products of food protein hydrolysis, free amino acids and short peptides, are the most potent chemical stimulants of the gastric phase of digestion. They are recognized by a variety of extracellular receptors belonging to the G-protein-coupled receptor superfamily, which are expressed by gastric mucosal exocrine and endocrine cells. Enteroendocrine G and D cells are likely the first level of integration of amino-acid-induced signals influencing a balance of endocrine activation and inhibition of gastric functions. This review focuses mainly on the physiological significance of dietary L-glutamate (Glu) in control of the gastric phase of digestion. The Glu signaling system in the stomach is linked to activation of the vagal afferents. In contrast to other natural amino acids, luminal Glu activates a paracrine cascade led by nitric oxide and followed by serotonin (5-HT), interacting in turn with 5- HT3 receptors on the afferent endings in the sub-mucosal layer. Glu, the only amino acid regularly ingested in a free form, enhances secretory and gastroprokinetic responses to protein- and amino-acid-rich diets but has no effect when applied alone or with carbohydrates. Possible mechanisms are discussed. © 2014 Bentham Science Publishers.

Ivanov K.P.,RAS Pavlov Institute of Physiology
Respiratory Physiology and Neurobiology | Year: 2013

Human lungs weighing ca 600. g permit the passage of 5-6. l of blood per minute. The blood capacity of the human lungs is about 0.5. l. Consequently, each 0.5. l of blood is during 5. s. The questions arise of how such a large mass of blood passes through such a small mass of lungs and what the reasons are for such a high rate of blood oxygenation. Since the structure of lungs in mammals is almost the same, we tried to solve these issues studying the rats, in which 20-22. ml of blood pass through the lungs of 1.5-2.0. g mass. A great blood flow appeared to be associated with a large diameter of the lung arterioles and a high rate of the blood flow in them. The high rate of oxygenation is accounted for by a special structure of alveoli and special conditions of the blood flow, which create ideal conditions for oxygen diffusion. © 2013 Elsevier B.V.

The present study provides evidence for anti-ictogenic activity of the mystixin 7 (MTX) mini-peptide in the pentylenetetrazole model of seizure. MTX was effective in inhibiting/suppressing ictal- and interictal-like activities over a long period of time (during 60-80. min). The peptide's anti-ictogenic effects were concentration- and time-dependent. An enzymatic treatment of MTX was accompanied by a decrease of the frequency pattern of epileptiform discharges, but their total blockade did not occurred. These findings indicate that the MTX mini-peptide has pronounced anti-ictogenic properties. © 2014 Elsevier B.V.

Danilova M.V.,RAS Pavlov Institute of Physiology
Journal of vision | Year: 2010

Are boundaries between color categories associated with enhanced discrimination? In the present experiments, chromatic thresholds were obtained for discriminations along lines orthogonal to the yellow-blue axis of color space. The targets were parafoveal and thresholds were measured with a spatial two-alternative forced choice. In interleaved experimental runs, we also obtained empirical estimates of the subjective yellow-blue line by asking observers to categorize colors as reddish or greenish. Both types of measurement were made in the presence of a steady background that was metameric to equal-energy white. In a limited region from desaturated yellow to desaturated blue, an enhanced discrimination is found near the subjective transition between reddish and greenish hues. This line of optimal discrimination is not aligned with either of the cardinal axes of color space: In a MacLeod-Boynton chromaticity diagram, it runs obliquely with negative slope.

Danilova M.V.,RAS Pavlov Institute of Physiology | Mollon J.D.,Downing St.
Vision Research | Year: 2012

Human color vision depends on the relative rates at which photons are absorbed by the three classes of retinal cone cell. The ratios of these cone absorptions can be represented in a continuous two-dimensional space, but human perception imposes discrete hue categories on this space. We ask whether discrimination is enhanced at the boundary between color categories, as it is at the boundary between speech sounds. Measuring foveal color discrimination under neutral conditions of adaptation, we find a region of enhanced discrimination in color space that corresponds approximately to the subjective category boundary between reddish and greenish hues. We suggest that these chromaticities are ones at which an opponent neural channel is in equilibrium. This channel would be 'non-cardinal', in that its signals would not correspond to either axis of the MacLeod-Boynton chromaticity diagram. © 2012 Elsevier Ltd.

Filaretova L.,RAS Pavlov Institute of Physiology
Therapeutic Advances in Chronic Disease | Year: 2011

Stress may contribute to the development and progression of gastrointestinal disorders. Activation of the hypothalamic-pituitary-adrenocortical (HPA) axis is one of the main characteristics of stress. For several decades it was generally accepted that glucocorticoids released during stress are ulcerogenic hormones. We designed some experimental studies in rats to clarify the validity of this widely held view. To achieve this goal, we examined the effect of glucocorticoid deficiency followed by corticosterone replacement or the glucocorticoid receptor antagonist, RU-38486, on stress-induced gastric erosion and the parameters of gastric function in rats. The data obtained shows that the reduction in the stress-induced corticosterone release, or its actions, aggravates stress-caused gastric erosion. It is suggested that an acute increase in corticosterone during stress protects the stomach against stress-induced injury. According to our results, various ulcerogenic stimuli, similar to stress, induce an increase in corticosterone that helps the gastric mucosa to resist against a harmful action of ulcerogenic stimuli. Glucocorticoids exhibit their gastroprotective effect by both maintaining local defensive factors and inhibiting pathogenic elements. Furthermore, the contribution of glucocorticoids to gastroprotection is tightly related to their contribution to general body homeostasis. Glucocorticoids provide gastroprotective actions in co-operation with prostaglandins, nitric oxide and capsaicin-sensitive sensory neurons. The results obtained do not support the traditional paradigm and suggest that glucocorticoids released during acute activation of the HPA axis are naturally occurring gastroprotective factors. In this article, we review our recent publications on the role of glucocorticoids in gastroprotection. © The Author(s), 2011.

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