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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.

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.

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.

Picrotoxin-induced kindling was shown to suppress the blastogenic response to bacterial lipopolysaccharide and phytogemagglutinin in male Wistar rats. The delta-sleep-inducing peptide as well as carbamazepine prevented the epileptogenic effects of picrotoxin. Carbamazepine was also effective against decreasing of phytogemagglutinin-induced blastogenic response.

In Wistar rats, the ED-50 of kainic acid induced clonic seizures. In early and postponed periods of kindling, the ED-50 decreased by 2,0 to 1.5 times. Kyotorphin did not affect the ED-50 of kainic acid in postponed periods.

The ED100 of the NMDA inducing clonic seizures (0.53 mcg) or tonic extension of forelimbs (5.02 mcg) increased their efficiency 2.3-fold and 4.46-fold, resp., due to the delta-sleep-inducing peptide administration in rats. The data obtained suggests a neuroprotective effect of the peptide on agonists of excitatory amino acid receptors action.

A seizure-protecting effect of the delta-sleep-inducing peptide (DSIP) and its analogues was revealed. An intensive sorption of H3 tryptophan occurred under the effect of the DSIP and its analogues. The data obtained suggests that the serotoninergic system plays no important part in the seizure-protecting effect.

An anti-ischemic effect of the delta-sleep-inducing peptide (DSIP) was found in rats. The DSIP effect was more obvious than that of the MK-801. The data obtained is discussed considering a possible use of the DSIP for brain stroke prophylaxis.

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.

Unilateral intranigral administration of a delta-sleep-induced peptide (DSIP) evoked a contralateral rotation. Naloxon prevented development of the effect whereas haloperidol administration enhanced the DSIP cataleptogenic effect.

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.

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.