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Aim: The characteristics of visual evoked potentials (VEP) have been studied in diabetic patients with and without diabetic retinopathy., Material and Methods: Magnetic impulses (2.0 T1 at the height of impulse) have been delivered to the cerebellar surface transcranially using the "Neuro-MS/D", (Russia Federation). Delta- sleep inducing peptide ("Deltalycyn", "Biopharma", Russia Federation) was intranasally delivered in 30 min before photostress. Afterwards VEP have been registered every 20 s from the moment of photo stress during one minute., Results: An increase of the latency period and a reduction of the VEP amplitude have been recorded in the period following photo stress exposure of the macular part of the retina. The VEP characteristics restored to the initial level in 73.5 +/- 3.3 s from the photo stress moment in the control group; while in diabetic patients with retinopathy this index was 137.2 +/- 11.3 s. In the. presence of cerebellar transcranial magnetic stimulations (2.0 T1, 20 impulses) the VEP amplitude depression was less pro- nounced, and the restoration period of the VEP characteristics shortened to 110.3+ 12.7 s, while in deltalycyn treated patients restoration was observed in 95.1+ 6.8 s. Under condition of combined usage of deltalycyn and TMS period of restoration of VEP was shortened up to 82.5 +/- 6.5 s., Conclusions: Retinopathy development is linked to prolonged VEP latency period (P100), lowering of the N75-P100 amplitude, as well as to enlargement of the recovery period of the retina's functional capacity in patients suffering from the diabetes mellitus in the presence of photo stress. Superlatively administered deltalycyn and cerebellar transcranial magnetic stimulation facilitates a faster recovery of the retina's functional capacity in response to photo stress in diabetic patients with retinopathy. 3. Combined usage of deltalycyn and cerebellar transcranial stimulation caused the potentiated shortening of post-photo stress recovering of VEP in patients with diabetic retinopathy.

The effects of valproate (VPA) and delta sleep-inducing peptide (DSIP) on metaphit-induced generalized, audiogenic seizure in adult rat males were compared. The animals were i.p. injected with: (1) Saline; (2) metaphit (mp, 10 mg kg(-1)); 3. metaphit (10 mg kg(-1)) and 8 h later with DSIP (0.1, 0.2, 0.4 or 1.0 mg kg(-1)), 4. metaphit (10 mg kg(-1)) and 8 h later with VPA (50, 75 or 100 mg kg(-1)); 5. DSIP alone (1.0 mg kg(-1)) and 6. VPA, alone (100 mg kg(-1)). The rats were exposed to sound stimulation at hourly intervals and the behavior and EEG were analyzed. The EEG signals in metaphit rats appeared as a sleep-like pattern and spike-wave complexes with increased power spectra. Valproate and DSIP reduced the incidence of seizure and prolonged duration of latency in a dose-dependent manner. ED50 of valproate in the 1st hour after administration was 63.19 mg kg(-1) and that of DSIP 3.19 mg kg(-1) four hours after injection. This suggests that VPA, reached a peak of action immediately after the application, while DSIP had a prolonged action, mildly reducing, but not abolishing metaphit seizure. None of the applied VPA and DSIP doses eliminated the metaphit-provoked EEG signs of epileptiform activity.

Local cerebral blood flow in the left hemisphere decreased most significantly in low-resistant Wistar rats preexposed to emotional stress. Deltaran selectively increased blood flow in the left hemisphere and improved blood supply to neuronal activity unit of the brain in these animals. This drug prevented progressive decrease in local cerebral blood flow in both hemispheres during the acute stage of ischemia. The effect of Deltaran was related to modulation of collateral blood flow and adequate blood supply to neuronal activity unit in the brain tissue. Deltaran decreased the mortality rate (by 62%) and alleviated the symptoms of cerebral ischemia. The positive effect of Deltaran was more pronounced in the left hemisphere.

Quantitative interferometry showed that chronic amphetamine administration to August rats (2.5 mg/kg/day for 3 weeks) increased the area of neuronal cytoplasm and nuclei and content and concentrations of proteins in hippocampal CA3 neurons. These changes persisted after single injection of delta sleep-inducing peptide (60 microg/kg). The reaction of the entire neuronal population of hippocampal CA3 neurons to amphetamine is similar.

The effect of delta-sleep-inducing peptide (DSIP) on the anticonvulsive activity of a nonprotective valproate (VPA) dose in a metaphit model of generalized, reflex audiogenic seizures in adult Wistar rats was studied. The animals that received metaphit (10 mg/kg) were exposed to audiogenic stimulation (100 +/- 3 dB, 60 s) at hourly intervals. Metaphit-treated rats displaying seizures in 8 previous tests were i.p. injected with VPA (50 mg/kg) or DSIP (1.0 mg/kg) or their combination. Latency to seizure was behaviorally assessed. The EEGs and power spectra were recorded and analyzed. Neurotoxicity was evaluated by the chimney test. DSIP or VPA alone expressed no significant effect on the latency duration, but their combination significantly prolonged latency to seizure during 6 h after injection, while inducing no significant motor impairment. Neither the applied drugs nor their combination abolished metaphit-provoked EEG epileptiform activity. The results show that DSIP potentiated anticonvulsive effects of a nonprotective VPA dose in a metaphit model of audiogenic seizures without influencing its neurotoxicity., (Copyright 2006 S. Karger AG, Basel.)

Problem: Previous studies have shown that humoral, endogenous and somnogenic, delta sleep-inducing peptide (DSIP) has influence on insomnia, pain, adaptation to stress, epilepsy, etc. We investigated the potential of DSIP and its analogue DSIP-12 (a nonapeptide with alanine in position 2 of DSIP molecule substituted by beta-alanine) to antagonize metaphit (1-[1(3-isothiocyanatophenyl)-cyclohexyl]piperidine) induced generalized, reflex audiogenic seizures in adult male Wistar albino rats., Methods: The rats divided in four groups received (i.p.): saline; metaphit; metaphit+DSIP; and metaphit+DSIP-12, respectively. Metaphit-treated animals displaying seizure in eight previous tests received DSIP or DSIP-12 and afterwards audiogenic stimuli were applied at hourly intervals for the next 30 h. The animals were exposed to sound stimulation 60 min after metaphit administration and further on at hourly intervals. Incidence and severity of seizures were behaviorally analyzed. Selected EEGs and power spectra were recorded and analyzed., Results and Conclusions: Metaphit led to hypersynchronous epileptiform activity (polyspikes and spike-wave complexes) and increased power spectra 0.5-30 h after the treatment. Severity of metaphit seizures increased with time to reach the peak 7-12 h after injection. DSIP and DSIP-12 significantly (*P<0.05 and **P<0.01) increased in delta and theta frequency bands and decreased the incidence, mean seizure grade and duration of metaphit convulsions. The results suggest that DSIP and DSIP-12 may be considered as potential antiepileptics in the animal model, DSIP-12 being more efficient than DSIP.

The effects of delta sleep-inducing peptide (DSIP) on metaphit- (1-(1(3-isothiocyanatophenyl)-cyclohexyl) (piperidine)-) induced audiogenic seizures in adult male Wistar rats were studied. The animals were divided into four experimental groups: 1. saline injected; 2. metaphit administered (10 mg x kg (-1)); 3. metaphit administered plus DSIP injected (dose range 0.1-1 mg x kg (-1)) and 4. DSIP injected (1 mg x kg (-1)). Upon treatment, the rats were exposed to sound stimulation ( 100 +/- 3 dB, 60 s) at hourly intervals and the incidence and severity (running, clonus and tonus) of seizures were analyzed. In most animals, metaphit led to EEG abnormalities and elicited epileptiform activity recorded as spikes, polyspikes and spike-wave complex and increased power spectra. Time-course studies revealed the peak of convulsive activity 7-12 h after the injection in metaphit-treated rats. DSIP acted as an anticonvulsant and the most potent anticonvulsive dose of 1 mg x kg (-1)significantly increased power spectra of deltawaves (2-11 h) in comparison with the saline-control group and decreased the incidence and duration of convulsive response, as well as mean seizure grade of metaphit-induced convulsions. These results suggest that DSIP should be considered as having potential anticonvulsant activity in this animal model., (Copyright 2002 Elsevier Science Ltd.)

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.

The influence of delta sleep-inducing peptide (DSIP) on sleep was studied in 16 chronic insomniac patients according to a double-blind matched-pairs parallel-groups design. Subjects slept for 5 consecutive nights in the laboratory. Night 1 was used for adaptation, night 2 for baseline measurements. In the afternoon before the 3rd, 4th and 5th night, half of the patients received intravenously 25 nmol/kg body weight DSIP, and half of the patients a glucose solution (placebo). Measures for sleep structure, objective (polysomnography) and subjective sleep quality and for subjective tiredness were assessed. The results for objective sleep quality indicated higher sleep efficiency and shorter sleep latency with DSIP as compared to placebo. One measure of subjectively estimated tiredness decreased within the DSIP group. Data analysis suggested, however, that the statistically significant effects were weak and in part could be due to an incidental change in the placebo group. As none of the other measures, including subjective sleep quality, showed any change, it was concluded that short-term treatment of chronic insomnia with DSIP is not likely to be of major therapeutic benefit.

The effects of delta sleep-inducing peptide (DSIP), on the sleep cycle of insomniac patients were assessed by means of polysomnographic recordings. DSIP in a dose of 25 nmol/kg or a placebo was administered i.v. during four nights using a double-blind crossover design. The number of nocturnal awakenings, non-rapid-eye-movement (NREM) sleep latency, total waking time and waking time after sleep onset were decreased under DSIP treatment, but no significant differences were found in comparison to baseline or to double-blind placebo nights. Total sleep time and NREM sleep time were increased by the peptide. Their increase was related to increases in stage 2, while stage 1, slow wave sleep (stages 3 and 4) and rapid-eye-movement sleep were not modified. For NREM sleep time and stage 2 sleep differences between DSIP and a placebo were significant, but the same differences existed already for the baseline values. It can be concluded that sleep improvement under DSIP treatment is of little clinical significance.

Impaired daytime functions are a significant part of chronic insomnia besides sleep disturbance. Therefore, the effects of intermediate-term delta-sleep-inducing peptide (DSIP) administration on sleep and daytime performance were investigated in 14 middle-aged chronic insomniacs. DSIP was administered under placebo-controlled, double-blind conditions for 7 successive nights. Polysomnograms were obtained for placebo baseline, beginning and end of DSIP treatment, and one placebo posttreatment night; daytime psychological state and mental performance were extensively tested before and after 6 DSIP injections. The treatment substantially improved night sleep with the first and additionally with repeated doses. These effects were maintained for the first posttreatment (placebo) night. Efficiency of night sleep and daytime rest reached the levels of normal controls. Alertness and performance at daytime increased significantly. The study demonstrates the efficacy of DSIP for the treatment of impaired sleep and daytime functions as well.

The effects of DSIP on night sleep and on waking functions are demonstrated in double-blind studies in insomniacs, presenting influences of single dose treatments as well as of repeated injections. Moreover, a single case study describes the efficiency of DSIP on narcolepsy.

The immediate effects of one week of Delta Sleep-Inducing Peptide (DSIP) administration (6 X 30 nmol/kg b.w., i.v.) and late effects after a follow-up period of one week were investigated in a sleep laboratory study. The population of 18 chronic psychophysiological insomniacs was subdivided into two groups of middle-aged (29-59) and older (60-83) insomniacs. In the middle-aged insomniacs, improvement of sleep to normal values occurred by the end of DSIP administration and was maintained during the follow-up week. In the elderly insomniacs, who showed an initial sleep disturbance double as severe as the middle-aged group, the immediate effect was larger, but full normalization of sleep was only obtained by the end of the follow-up period. Although there was an interaction of sleep pathology and age, a regression analysis yielded clear evidence that the effects of DSIP were correlated to the degree of sleep disturbance. The whole sample of insomniacs showed normal sleep patterns at the end of the investigation.