Interactions of excitation foci and their complexes in cerebral cortex.
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Acetylcholine↗
Biomedical subjects
A A Shandra
Publications and source records attributed to A A Shandra.
The influence of the delta-sleep-inducing peptide on convulsive activity.
Data are presented in this paper on the influence of the delta-sleep-inducing peptide (DSIP) on various forms of convulsive activity. The capacity of this peptide to suppress convulsive activity in foci created in the cerebral cortex by the application of strychnine has been demonstrated in experiments on cats. It has been established in experiments on rats that DSIP determines the later development of the convulsive kindling syndrome, and prevents the development of convulsions in mice induced by bicuculline, picrotoxin, and corazol, but is devoid of such action in relation to thiosemicarbazide and strychnine. It was demonstrated that the anticonvulsant action of DSIP is associated with its influence on the reticular portion of the substantia nigra. The lowest level of this peptide itself has been discovered, in the reticular portion of the substantia nigra at the late stages of pharmacological kindling. It is inferred that DSIP may represent one of the factors of the endogenous control of the excitability of the brain.
Animals↗
Role of hyperactive determinant structures in the creation of functional complexes of seizure activity in the cerebral cortex.
Foci of enhanced excitability, with independent discharge patterns, were created by subconvulsive strychninization in experiments on cats. A focus of more powerful excitation created with the same strychnine played the role of determinant despatch station (DDS). Its importance is that it determines the character of activity of the other foci of excitation, strengthens excitation in them, combines them into a single functional complex, and determines the character of activity of the whole complex. This complex can be destroyed by suppressing the DDS with pentobarbital. Blocking individual destination stations included in the complex does not lead to its destruction.
Animals↗
Role of adrenoreactive structures of the amygdaloid complex in the regulation of blood coagulation.
The stimulation of alpha-adrenoreactive structures of the amygdaloid complex, both in isolation and against the background of disengaged beta-adrenoreactive structures, was carried in experiments on male cats in chronic experimental conditions through an implanted chemotrode. It was shown that the alpha-adrenoreactive structures of the amygdaloid complex exert an influence mainly on blood coagulation phases I-II. Blood coagulation phase III changes indirectly through the shortening of phases I-II. The stimulation of beta-adrenoreactive structures of the amygdaloid complex induces the elongation of blood coagulation phases I-III over the duration of the entire experiment. The stimulation of these structures in conditions of the disengagement of the alpha-adrenoreactive structures of the amygdala leads to insignificant changes in phases I-II, after which a hypercoagulation effect is observed. Blood coagulation phase III in these conditions reflects a marked hypocoagulation effect. The data obtained suggest a modulating role of the adrenoreactive structures of the amygdaloid complex in the regulation of the processes of blood coagulation.
Amygdala↗
Use of nicotinamide and pyridoxal-5-phosphate in the treatment of experimental epilepsy.
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Animals↗
Effect of intranigral dosage with delta-sleep-inducing peptide and its analogs on movement and convulsive activity in rats.
Studies were carried out in rats on the effects of the administration of delta-sleep-inducing peptide (DSIP) and its analogs (1-4) into the reticular part of the substantia nigra on movement and convulsive activity. Intranigral microinjection of DSIP, and of DSIP-1 and DSIP-4, reduced horizontal and vertical movement activity as well as excursions to the center of the open field. DSIP, DSIP-2, and DSIP-3 had anticonvulsant effects, consisting of increases in the latent periods of the first convulsion and clonicotonic convulsions induced by picrotoxin, and reductions in the mean intensity of convulsions. It is suggested that changes in the structure of DSIP are accompanied by alterations in the strength of the effects of this peptide on horizontal and convulsive activity after dosage into the reticular part of the substantia nigra. The results indicating that these peptides have protective activity in experimental convulsive syndrome suggest that a relationship exists between DSIP-induced reductions in movement activity and the anticonvulsive efficacy of DSIP analogs when administered intranigrally, this being one of the components of the nigrodependent mechanisms of inhibition of convulsions.
Animals↗
Influence of the neuropeptide galanin on active avoidance in rats.
It was demonstrated in experiments on rats that the injection of the neuropeptide, galanin (200, 500, and 1000 ng), into the lateral cerebral ventricles induced a dose-dependent decrease in the number of successful attempts at avoidance in rats trained preliminarily to active avoidance by jumping. The preliminary administration of the cholinolytic, atropine (1 mg/kg, intraperitoneally), to the rats also caused an acceleration of the damping of the conditioned reflex and potentiated the indicated effect of galanin during the experiment. The use of the opioid antagonist, naloxone (1 mg/kg, intraperitoneally), did not exert an influence on the animals' behavior, but blocked the galanin-provoked acceleration of the extinction of the active avoidance habit. The intraperitoneal administration of a noncompetitive antagonist of excitatory amino acids, ketamine (10 mg/kg), did not influence the character of the animals' behavior nor the indicated effects of galanin. It was concluded that galanin possesses an amnestic action in the active avoidance test, and that this effect of the peptide is determined by the suppression of cholinergic and activation of opiatergic transmission in the central nervous system.
Animals↗
Effects of delta-sleep-inducing peptide on NMDA-induced convulsive activity in rats.
Acute experiments on rats showed that the ED100 of NMDA for induction of clonic convulsions was 0.53 microgram, while the ED100 of NMDA for inducing tonic extension of the forelimbs was 5.02 micrograms/animal. Determination of these parameters after administration of delta-sleep-inducing peptide (100 micrograms/kg, i.p.) revealed 2.3- and 4.46-fold increases. These results provide evidence for a neuroprotective role of delta-sleep-inducing peptide in relation to excitatory amino acid receptor agonists.
Animals↗
Delta-sleep-inducing peptide and its analogs and the serotoninergic system in the development of anticonvulsive influences.
Experiments on rats were carried out to study the effects of administration of delta-sleep-inducing peptide (DSIP) and its analogs (9-14) into the reticular part of the substantia nigra and ventral hippocampus on picrotoxin- and kainate-induced epileptic activity. Additionally, the uptake of [3H]tryptophan by brain structures was studied. Intranigral and intrahippocampal microinjections of peptide and its analogs were found to have anticonvulsant effects against both picrotoxin- and kainate-induced epileptic activity. Studies of the effects of DSIP and its structural analogs on the uptake of tryptophan by brain structures showed that peptides predominantly increased uptake of this amino acid. It is suggested that brain structures which modulate tryptophan uptake are largely responsible for the anticonvulsant actions of DSIP and its analogs. The results obtained here provide evidence that the serotoninergic system is not of key importance in mediating the anticonvulsant effects of DSIP and its analogs.
Animals↗
Effects of delta-sleep-inducing peptide in cerebral ischemia in rats.
Experimental studies were carried out to investigate the neuroprotective effects of delta sleep-inducing peptide in animals with cerebral ischemia induced by bilateral compression of both carotid arteries, and to compare the efficacy of this peptide with that of MK-801. These studies led to the conclusion that the peptide had pronounced anti-ischemic effects, which were evident within 24 h and consisted of reductions in the severity of postural abnormalities in rats with bilateral cerebral ischemia, along with a reduction in lethality. Comparison of the efficacies of peptide and MK-801 showed the peptide to have the greater neuroprotective effect. These results are regarded as providing an experimental basis for using the peptide as a therapeutic agent in patients with stroke.
Animals↗
Antiepileptic properties of cerebrospinal fluid after activation of the antiepileptic system of the brain.
Intraventricular injection of cerebrospinal fluid (CSF) obtained from cats with chronic electrical stimulation of cerebellar vermal cortex resulted in suppression of epileptic foci activity in cat brain cortex, an increase in time to first seizure, and weakening of generalized seizures in rats. The CSF obtained from cats after electroshock seizures induced less pronounced, although significant antiepileptic action in comparison with the CSF of cats with cerebellar stimulation on the model of generalized seizures in rats. The antiepileptic action of CSF obtained from cats with electrostimulation of cerebellar vermis and from electroshock cats is due to appearance of peptide factors in CSF.
Animals↗
[Role of functional interrelationships of the adrenoreactive structures of the amygdalar complex and vascular walls in the regulation of blood coagulation].
The chronic experiments on 24 male cats were carried out to study the influence of changes in functional interrelations between alpha- and beta-adrenoreactive amygdalar structures and corresponding receptors of vascular wall upon haemostatic system. It is shown that activation of alpha-adrenoreactive structures causes the hypercoagulative effect and that of beta-adrenoreactive receptors--the hypocoagulation activation. The central adrenoreactive structures realize their regulative influences through corresponding peripheral adrenoreceptors of the vascular wall.
Amygdala↗
[The effect of the cerebrospinal fluid from rats subjected to picrotoxin-induced kindling on the motor activity and seizure susceptibility of recipient animals].
Experiments on rats have shown that repeated administration of primarily subthreshold dose of picrotoxin leads to the occurrence and progressive enhancement of seizure manifestations. During picrotoxin kindling the decrease of locomotor activity in interictal periods was recorded. Microinjection of cerebrospinal fluid (CSF) of kindled rats into lateral brain ventriculi of recipients resulted in decrease of locomotor activity and acute primarily generalized picrotoxin induced seizures. These effects of CSF were blocked by naloxone administration and were observed only if injecting CSF which was preliminarily treated with protease inhibitors. It is concluded that endogenous opioid substances accumulate in CNS during kindling and evoke a decrease in the locomotor activity. These substances act as anticonvulsant factors which control the development of epileptic activity.
Animals↗
[The effect of cerebellar structures on the epileptic activity in the brain].
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Animals↗
[Kindling as a model for the formation of behavioral disorders].
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Animals↗
[Changes in the sleep-wakefulness cycle in experimental Parkinson's syndrome].
It was demonstrated in rat experiments that in modelling the akinetico-rigid parkinsonian syndrome by injecting kainic acid into the caudate nuclei the phases of wakefulness and light slow-wave sleep decreased while the phase of deep slow-wave sleep increased. In the tremorogenic from of the parkinsonian syndrome induced by reserpine the phases of wakefulness and deep slow-wave sleep decreased in the rats while the phases of light slow-wave and paradoxical sleep increased. In destruction of the substantia nigra with kainic acid the phase of paradoxical sleep reduced. The results of the study are discussed from the standpoint of the generator mechanisms of the development of neuropathological syndromes and the mechanisms of the interrelations of parkinsonism and epilepsy.
Animals↗
[Effect of low-frequency electric stimulation of the dentate nucleus of the cerebellum on foci of epileptic activity].
It was demonstrated in acute experiments on cats that low-frequency (7-12 Hz) electrical stimulation of the dentate nucleus of the cerebellum induces the formation of ictal discharges in foci of powerful epileptic activity produced in the brain cortex by application of penicillin solution. Ictal discharges were also provoked under the effect of electrical stimulation (7-12 Hz) of the ventrolateral nucleus of the thalamus. Destruction of the ventrolateral nucleus abolished the effect of ictal discharge facilitation induced by stimulation of the dentate nucleus. The results are discussed from the standpoint of increasing the efficacy of the stimulation method for arresting the epileptic syndrome.
Animals↗