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Biomedical subjects

N E Chepurnova

Publications and source records attributed to N E Chepurnova.

At least 37 records · Page 2Linked to original sources

[Effect of melanostatin on the central nervous system].

The effect of melanostatin (MIF), L-DOPA and morphine on the behaviour and electrical activity in the neocortex and lymbic structures in rats has been strudied. All substances were administered intraventricularly. There was a recorded increase of the energy of the delta and theta slow waves in the hypothalamus, amygdala and neocortex and also of the energy of the alfa waves in the amygdala and neocortex. In addition the administration of L-DOPA and morphine facilitated the effect of MIF while preliminary administration of MIF blocked the effect of morphine given in threshold doses.

Animals↗

[Evoked potentials in the rabbit amygdala following its partial deafferentation].

The EPs in the rabbit Amygdala were recorded after chronic (5 weeks) deafferentation following section of stria terminalis, commissura anterior and the ipsilateral frontal lobe cortex. Stimulation of the bulbar olfactory regions caused some facilitation of the EPs in non-olfactory nucleus of amygdala. Following ventromedial hypothalamic stimulation, the EPs remained unchanged in the caudal parts, diminished in the rostral parts of basolateral amygdala and disappeared in the medial nucleus of amygdala.

Amygdala↗

[Effect of somatostatin on neurons of partially deafferented amygdala in the rabbit].

Responses of 291 neurons to microelectrophoretically injected somatostatin were studied in the amygdala of rabbits under nembutal anesthesia. Both excitatory and inhibitory effects were found in contrast to earlier data on the only inhibitory reactions in hypothalamic neurons. After partial chronical deafferentation of the amygdala responses to somatostatin application were observed in 76% of the registered neurons, 90% of these neurons with background discharge frequency from 6 to 20 imp/s, responded by an increase in their activity, while inhibitory reactions were recorded in neurons with average background discharge frequency above 20 imp/s. Since amygdaloid neurons exert a regulating effect on the secretion of the growth hormone through somatostatin, it is suggested that the observed responses reflect one of their feedback mechanisms.

Afferent Pathways↗

Peptidergic mechanisms of hyperthermia-evoked convulsions in rats in early postnatal ontogenesis.

This report addresses the verification of the hypothesis that arginine-vasopressin affects the formation of hyperthermia-evoked convulsions in early ontogenesis in rats on days 3, 5, 7, and 9 of postnatal life. The modification of experimental febrile convulsions by PACAP (pituitary adenylate cyclase-activating peptide) was investigated; PACAP is a physiological regulator of the neurosecretion of arginine-vasopressin. Arginine-vasopressin (10 microg/rat) and PACAP (0.01 microg/rat) decreased the latency of generalized tonic-clonic convulsions and the time of truncal generalization of convulsive activity on days 3 and 5 of rat development. Animals given arginine-vasopressin (0.1-10 microg/rat) sowed significant increases in the duration of generalized convulsions to the level of status epilepticus on day 9 of life. Conversely, administration of higher doses of PACAP (0.1 microg/rat) increased the threshold of tonic-clonic convulsions on days 3 and 5 and decreased it on days 7 and 9 of postnatal development. The indirect involvement of PACAP in the mechanisms of experimental febrile convulsions is suggested to act via changes in arginine-vasopressin neurosecretion.

Animals↗

[Pituitary adenylate cyclase activating peptide (PACAP)--its polyfunctionality in the mechanisms of brain protection].

Modern data of molecular and biological properties and physiological role of new pituitary adenylate cyclase activating polypeptide--PACAP--review. PACAP play key role in the embryogenesis of brain, in the protection of brain nerve cells from ischemia-induced death, injuring and apoptosis. New data are discussed concerned with molecular cloning and tissue distribution of receptors for PACAP, gene proPACAP expression in gastrointestinal tract, reproductive organs and nervous system. PACAP increase cytosolic free calcium and modifies the calcium-sensitive K(+)-channels, PACAP protects cultures cortical and hippocampal neurons from glutamate-induced cytotoxicity. The sleep modulation and modification of seizures activity of brain through the secretion of vasopressin or/and through NMDA receptors directly should be include in the program of PACAP "physiological continuum" of functions.

Amino Acid Sequence↗

[Anxiety and behavior in WAG/Rij strain rats with genetically induced absence attacks].

Behavior of nonlinear rats and animals from Wistar and WAG/Rij (with inborn generalized absence epilepsy) strains was examined in the elevated plus-maze and the hole board. WAG/Rij rats demonstrated low exploratory behavior in both tests. In the elevated plus-maze, WAG/Rij rats were more balanced and more anxious than Wistar and nonlinear rats. Administration of ethosuximide completely eliminated spike-wave discharges but did not change behavioral interstrain differences. Since the spike-wave patterns develop in WAG/Rij at the age of 3 months, the behavior of young (2-moth-old) pups from different strains was compared and significant differences were revealed. Correlation between the genetically defined features (spike-wave discharges) and behavioral peculiarities in WAG/Rij rats is supposed.

Aging↗

[The piriform cortex and the cortical nucleus of the amygdala in epileptogenesis--the role of the rostrocaudal gradient].

The seizure susceptibility of amygdaloid complex in rat was investigated. In piriform cortex and cortical nucleus of amygdaloid complex the structural and electrophysiological rostro-caudal differences were found (using relative spectral densities EEG, seizure thresholds, electrical kindling rate). The fundamental dependence of severity of motor seizures from structural (nuclear or cortical) organization of stimulating area was shown. There were more of limbic stages while stimulating anterior and posterior cortical nuclei, and there were more generalized stages while stimulating piriform and periamygdaloid cortex. Using the model of electrical kindling anticonvulsant effects of Sacricin were demonstrated. Sacricin is one of the compounds of polycarbonic acid. Sacricin has fully coped the process of secondary generalization of epileptic seizures.

Amygdala↗

[Neuropeptide thyroliberin--an endogenous anticonvulsant in the brain].

Thyroliberin (TRH) promoting endogenous antidepressive effect is the most general regulator of the central mechanisms and visceral functions (especially respiration). Our group pioneered in applying the anticonvulsant action of TRH after local intranasal application. This application TRH in ultra-low doses contrast the method of systemic TRH administration (i.v., i.m. or oral in the large doses--mg). In our experiments intranasal application of 10(-9) M, 10(-10) M and 10(-12) M TRH significantly inhibited the severe epileptic motor fits in rats induced by pentylenetetrazole (PTZ). Beneficent effect of TRH is also confirmed by EEG (TRH suppressed SWD in cortex, amygdala and hippocamp). In the experiment that follows compared effects of TRH (pyroGlu-His-Pro-NH2) and its metabolite dipeptide cHis-Pro-NH2 (10(-10) M, 10(-5) M). The experiments make more precise that only TRH but not His-Pro posses the anticonvulsant properties. There is a good believe that medical potentialities of TRH have not been exhausted and its new possibilities of its usage will be revealed in epileptology.

Animals↗

[Hippocampal ripple oscillations (200 Hz) in mechanisms of memory consolidation].

A current status of knowledge about high-frequency (140-200 Hz) ripple oscillations in the CA1 hippocampal subfield is summarized and considered in the context of two-stage model of the hippocampal memory processing. A large body of evidence suggests highly-selective recruitment of pyramidal cells and interneurons in the generation of the oscillatory pattern after co-operative sharp-wave-related discharge of CA3 pyramidal neurons. We also discuss a role of transmission via gap junctions in the mechanisms of ripple oscillations as well as their adaptive aminergic (histaminergic) modulation. Patterns of neuronal firing in the hippocampus observed during ripple oscillations reproduce space-dependant neuronal activity from the previous waking period. Together with a data about efficacy of high-frequency stimulation for induction of synaptic modification it points out a role for ripples in the formation of long-term memory. Focal ultra fast ripples (up to 500 Hz) have been shown to participate in the development of temporal lobe epilepsy.

Animals↗

[Cholinergic mechanisms in the pathogenesis of genetically-caused absence epilepsy].

Frontoparietal cortex and the thalamocortical circuit comprising reticular thalamic nucleus (RTN) and relay nuclei of the ventrolateral thalamus (VLT) are critical structures in the generation of spike-wave discharges (SWD) during absence seizures. The activity of these nuclei is under the control of the ascending cholinergic projections of nucleus basalis of Meynert. The aim of our study is to make an attempt to change the pattern of SWD in WAG/Rij rats by injecting of cholinotoxine AF64A to the area of RTN. Spontaneous SWD were registered in cortex of WAG/Rij rats with genetically determined absences. The spectral content of SWD was analyzed by means of the Fast Fourier Transformation (FFT) procedure. Unilateral injections of AF64A (1 nmol) to RTN led the decrease in duration and number of SWD comparing to the basal EEG recordings 2 days after the lesion. The FFT analysis showed the disappearance of 17-18 Hz spike on the side of the lesion compared with the intact side. The immunohistochemical study for acetylcholinetransferase (ChaT)-containing neurons showed the loss of ChaT-positive cells in the nucleus basalis area on the side of the lesion. The removal of cholinergic afferentation of RTN and cortex from nucleus basalis inhibits the SWD developing most likely due to the decrease of cortical excitability. Moreover, possibly cholinergic transmission is involved in the transforation of the synchronized phenomena (SWD) to another with close mechanism of generation.

Animals↗

[Neuropeptide thyroliberin in ultra low doses--anticonvulsant defense of the brain].

Thyroliberin (TRH) promoting endogeneous antidepressive effect is the most general regulator of the central mechanisms and visceral functions (especially respiration). Our group pioneered in applying the anticonvulsant action of TRH after local intranasal application). This application of TRH in ultra-low doses contrast the method of systemic TRH administration in the large doses). In our experiments intranasal application of 10(-8), 10(-10) and 10(-12) mol/l TRH significantly inhibited the severe epileptic motor fits in rats induced by PTZ. EEG also confirms beneficent effect of TRH (TRH suppressed SWD in cortex, amygdala and hippocamp). In the experiment that follows compared effects of TRH (pyroGlu-His-Pro-NH2) and its metabolite dipeptide His-Pro (10(-10), 10(-8) mol/l). The experiments make more precise that only TRH but not His-Pro posses the anticonvulsant properties. There is a good believe that medical potentialities of TRH have not been exhausted and its new possibilities of its usage will be revealed in epileptology.

Administration, Intranasal↗

[The cortico-thalamic theory for generalised spike-wave discharges].

The origin of generalized absence epilepsy is still not known. In the last century, four theories have dominated the debate about the origin of the bilateral synchronous generalized spike-wave discharges associated with absence seizures: the "centrencephalic" theory [Penfield and Jasper], the "cortical" [Bancaud, Niedermeyer, Luders], the "cortico-reticular" theory [Gloor, Kostop[oulos, Avoli] and the "thalamic clock" theory [Buzsaki]. There is now some evidence that absence epilepsy, as studied in the WAG/Rij model, is a corticothalamic type of epilepsy. A new hypothesis is proposed which suggests that a cortical focus in the somatosensory cortex is driving the widespread corticothalamic networks during spontaneous absence seizures. This modern theory was given the name "hot spot' theory" [Meeren et al., 2002]. According to the present view three brain structures are critically involved and their integrity seems a minimal and sufficient condition for the occurrence of spike-wave discharges. Firstly, the reticular thalamic nucleus is involved and most likely its rostral pole. Secondly, the thalamocortical relay cells in the ventrobasal complex play a role and, thirdly and most importantly, the cerebral cortex with its epileptic zone. The zone in which the epileptic focus seems to be localised is located on the somato-sensory cortex, and more precisely in the area on which the peri-oral region including the upper lip, projects.

Animals↗