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Biomedical subjects

A A Shandra

Publications and source records attributed to A A Shandra.

At least 19 recordsLinked to original sources
PubMed2002

The role of TNF-alpha in amygdala kindled rats.

In the present study, the interaction between epileptogenesis and the immune system were studied in a kindling model. First, the effects of a single administration of TNF-alpha (5.0 microg/kg, i.p.) on seizure and EEG activity were investigated in amygdala-kindled rats. TNF-alpha treated rats showed more prolonged epileptiformic discharges than control rats. TNF-alpha also induced a decrease in the power of delta band and an increase in theta and alpha activity. In addition, a marked increase in the power of beta and gamma band was observed. The EEG changes were most numerous in the frontal cortex and amygdala. All effects were registered 24 h after TNF-alpha administration. Finally, electrical stimulation enhanced the level of TNF-alpha in blood serum from 1.9 +/- 1.5 to 12.7 +/- 3.8 pg/ml and in brain tissue 56.8 +/- 6.0 to 109.2 +/- 6.0 pg/mg, as was determined via the ELISA method. It can be concluded that there is a mutual facilitative interaction of both epileptogenic and cytokine-derived mechanisms on this type of seizure. The changes in the power spectrum of the EEG after TNF-alpha might contribute to intensify thalamic-derived facilitation of epileptic discharge in cortical structures.

Amygdala↗
PubMed2002

Causes and consequences of pathogenic processes in evolution: implications from experimental epilepsy in animals.

Examples from experimental epilepsy in animals are used to illustrate the view that a crucial role of the transfer of mechanisms from compensatory into pathogenic (e.g. lethal ones in the course of a disease), is played by the power of pathologic stimuli. In the genesis of epilepsy it is suggested that a critical increase of endogenous factors may underlie the conversion of the absence form of epilepsy into a generalized self-supporting form. The ability to precipitate endogenous self-augmenting mechanisms of diseases may have increased in the course of evolution. The lethal result of a serious pathogenic process leads to the suggestion that organisms cope with the disease by dying. This prevents spreading of the putative infectious disease within the population. This mechanism of disease aggravation could play a role in the survival of the species and in further evolutionary progress. This may explain why certain species may have survived in evolution and supports the theory of synthetic evolution.

Animals↗
PubMed1996

Chemical kindling: implications for antiepileptic drugs - sensitive and resistant epilepsy models.

The efficacy of phenobarbital (PB) and phenytoin (PHT) was evaluated against the convulsions in chemically (picrotoxin, PTX) kindled rats. Two protocols were used: assessment of seizures immediately after the completion of the kindling procedure and after the 2-week postkindling PTX-free period, as compared with acute PTX seizures. Kindled convulsions were more sensitive than acute PTX seizures to the antiepileptic action of PB and PHT. On the other hand, the "postkindling state" was characterized by the enhancement of the severity of the convulsions in comparison with both kindled and acute PTX seizures and dramatic increase in the resistance to the action of antiepileptic drugs (AEDs). It is concluded that the two paradigms--kindling proper and "postkindling"--could be applied as models for AED-sensitive and AED-resistant animal epilepsy models correspondingly.

Animals↗
PubMed1995

Seizure-protecting effects of kyotorphin and related peptides in an animal model of epilepsy.

Administration of peptides kyotorphin (KT), neokyotorphin (NKT), and d-ser-2-NKT into the lateral brain ventricle (10 nmol) increased the latency and attenuated the severity of picrotoxin-induced convulsions in rats. Anticonvulsive effects of the peptides were also observed after their administration into the CA1 hippocampi (2.5, 5, 10 nmol), with the order of potency d-ser-2-NKT-->NKT-->KT. When injected into the substantia nigra reticulata, the 10 nmol dose of NKT and d-ser-2-NKT displayed equal seizure-protecting effect, which was higher than that for KT. It is concluded that kyotorphin and its analogs provide structure-dependent, dose-dependent, and target site-dependent antiepileptic effect.

Analgesics↗
PubMed1995

[The effect of the intranigral use of the delta sleep-inducing peptide and its analogs on the motor and seizure activities of rats].

The effects of delta-sleep inducing peptide (DSIP) and its analogues (1-4) administered into substantia nigra pars reticulata on locomotor and seizure activity were estimated in experiments in rats. It was shown that intranigral microinjection of DSIP as well as DSIP-1-DSIP-4 caused decreasing of horizontal, vertical locomotor activity and attendance of central sectors of the "open field". Antiseizure effects, i.e. the first and clonic-tonic picrotoxin-induced convulsive latent period lengthening and their intensity decreasing, revealed DSIP, DSIP-2 and DSIP-3. Authors suppose that changes of DSIP structure lead to changes of effects expression on locomotor and seizure activity in conditions of their administration into substantia nigra reticulata. Obtained data concerning protective effects of studied peptides on experimental seizure syndrome allow to conclude that there is interaction between DSIP-induced hypokinesia and DSIP analogues anticonvulsive effectiveness in case of their intranigral administration which is likelihood is one of the component of nigral-dependent seizure-suppressive mechanism.

Animals↗
PubMed1995

[The role of the delta sleep-inducing peptide in the formation of neuropathological syndromes].

The authors considered the pathogenetic role of delta-sleep inducing peptide (DSIP) in different neuropathological syndromes development and manifestation. According to own as well as published in the literature data authors showed the parkinsonian and the rotational syndromes development following DSIP central administration. Briefly, DSIP is a neuropeptide which play significant role in the mechanisms of development of different neuropathological syndromes, namely, epileptic, parkinsonian, withdrawal, rotational and others syndromes.

Animals↗
PubMed1994

On the mechanism of antiepileptic peptides appearance in the cerebrospinal fluid.

Intraventricular injection of cerebrospinal fluid obtained from cats with electroshock seizures resulted in suppression of generalized picrotoxin-induced seizures in rats. Antiepileptic action of cerebrospinal fluid was abolished by partial bilateral midbrain destruction that included the region of colliculi superii. Electrical stimulation of cerebellum in cats with such destructions caused the appearance of a pronase-sensitive antiepileptic substances in cerebrospinal fluid.

Animals↗
PubMed1993

[The effect of the neuropeptide galanin on active avoidance in rats].

Administration of galanin into the lateral brain ventricles induced a dose-dependent impairment of memory in the active avoidance test in rats. Atropine both induced the impairment of memory and potentiated the galanin amnestic effect. Naloxone had no such action as well as ketamine. Galanin seems to impair memory via suppressing cholinergic and activating opioid peptidergic transmission in the CNS.

Animals↗
PubMed1993

[The effect of galanin on the experimental parkinsonian syndrome in rats induced by the intrastriatal administration of kainic acid].

Experiments in rats showed that intrastriatal administration of kainic acid in a dose of 100 but not 20 ng per side resulted in the development of behavioral disorders reminding those of Parkinsonian syndrome: bradykinesia, increased muscle rigidity, ptosis. Intrastriatal administration of galanin in doses of 10 and 50 ng induced only a decrease of locomotor activity in the "open field". When co-administered with kainic acid (20 ng), galanin displayed a dose-dependent potentiation of behavioral Parkinsonian-like disturbances the severity of which increased depending on the dose used. It is concluded that galanin potentiates the kainic acid-induced development of the generator of pathologically enhanced excitation in the striatum underlying the mechanisms of Parkinsonian syndrome. Thus, the increased galaninergic striatal activity could participate in the mechanisms of the above-mentioned CNS disorders.

Animals↗
PubMed1993

[The effect of the electrical stimulation of the superior colliculli on focal epileptic activity in the cerebral cortex ].

Acute experiments in rats showed that SC electrical stimulation (ES) (100 Hz, 5 V, 0.25 ms) resulted in suppression of the epileptic activity in contralateral strychnine-induced (0.1%; 1.0%) focus and shortening of the focus existence time. After electrocoagulation of SC ES-zone the EpA in the focus was restored. ES of SC ipsilateral to strychnine-induced (0.1%) focus caused an increase in the spike frequencies but significant part of the antiepileptic system.

Action Potentials↗
PubMed1993

[Synthesis and biological properties of new analogs of delta-sleep peptide. I. Antiepileptic effect].

To study structure-functional relationship in the series of DSIP, eleven DSIP analogues varying in positions 1, 2 and 6 were synthesized by the solid-phase method using both Boc- and Fmoc-approaches. The antiepileptic action of these analogues was compared with that of DSIP. The seizure activity was induced by the corazol or picrotoxin i. p. injection. Some analogues proved more efficient as antiepileptic agents than DSIP after their central (50 micrograms/kg in rats) and peripheral (1.0 mg/kg in mice) administration.

Amino Acid Sequence↗
PubMed1992

[Role of limbic structures in the mechanisms of post-traumatic epilepsy].

It was shown in the experiments on rats that intracerebroventricular administration of kainic acid (0.01, 0.05 microgram) after brain trauma, resulted in the occurrence of behavioral and electrographic convulsive disturbances; maximal expression of epileptic activity was obtained in entorhinal cortex and ventral hippocampus. Kainic acid induced epileptic reactions in nontraumatized rats only if injected in dose 0.1 microgram. Brain trauma did not lead to changes in seizures intensity induced by systemic picrotoxin administration. It is concluded that the formation of generator of pathologically enhanced excitation in limbic structures via increase of excitor glutamatergic neurotransmission is the important mechanism of traumatic epilepsy.

Animals↗