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Biomedical subjects

M Radulovacki

Publications and source records attributed to M Radulovacki.

At least 73 records · Page 4Linked to original sources
PubMed1982

Quipazine has a biphasic effect on slow wave sleep and reduces REM sleep rebound in REM sleep deprived rats.

Rats implanted with electrodes for polygraphic recording were deprived of REM sleep for 24 hr. Following REM sleep deprivation animals were injected with quipazine maleate (7.5 mg/kg IP) and were polygraphically recorded for 48 hr. The results show that quipazine reduces REM sleep rebound and that it has a biphasic effect on slow-wave sleep: initial 6 hr suppression is followed by a delayed increase in the second 24 hr recording period. The initial suppression of slow-wave sleep we attribute to the stimulation of central serotonergic receptors while the effect on REM sleep rebound may result from quipazine's action on central catecholamines.

Animals↗
PubMed1981

Sleep suppressant action of quipazine: relation to central serotonergic stimulation.

Administration of quipazine maleate (1-10 mg/kg, IP), a proposed 5-hydroxytryptamine (5-HT) receptor stimulant to rats produced a dose-related suppression of both slow-wave sleep (SWS) and rapid-eye-movement sleep (REMS) accompanied by an increase in head-shaking behavior. These effects were observed during the first 6 hr of a 12-hr EEG recording session. The latencies to the sleep states were markedly prolonged and correlated with the duration of head-shaking behavior induced by the drug. A significant inverse relationship was found between the amount of SWS or REMS and the number of head-shakes occurring during the first 6-hr period. Since head-shaking behavior in rodents has been proposed as a quantitative, behavioral model of central 5-HT activation, the data suggest a causal relationship between enhanced 5-HT activity and sleep suppression. This assumption is further supported by the observation that pretreatment with metergoline (2.5 mg/kg, IP) a 5-HT receptor blocker, reduced quipazine's effects on both SWS and head-shaking behavior.

Animals↗
PubMed1981

Phenoxybenzamine and bromocriptine attenuate need for REM sleep in rats.

Phenoxybenzamine (10 mg/kg, IP), an alpha-adrenoreceptor blocker, and bromocriptine (5 mg/kg, IP), a dopamine receptor stimulant, were administered to rats while the animals were being deprived of REM sleep by selective REM sleep deprivation method. We have shown recently that alpha-adrenoreceptor blockers and bromocriptine when administered to rats after the animals had been deprived of REM sleep were able to abolish REM sleep rebound and thus attenuate the need for REM sleep. The purpose of this study was to investigate whether these agents might also have the capacity to attenuate the need for REM sleep when given to animals in a situation when the need for REM sleep is being generated, i.e. during REM sleep deprivation. Our results show that administration of phenoxybenzamine or bromocriptine to rats immediately before or during the period of REM sleep deprivation also abolished appearance of subsequent REM sleep rebound. This suggests that administration of the two pharmacological agents prevented the generation of REM sleep pressure by fulfilling the need for REM sleep.

Animals↗
PubMed1981

Bromocriptine, dihydroergotoxine and sleep in rats: effects of repeated administration.

Bromocriptine mesylate (7.5 mg/kg, i.p.) and dihydroergotoxine mesylate (DHET); 3 mg/kg, i.p.) were administered 4 times at 9-hour intervals within a 27-hour period to rats polygraphically recorded for 84 h. Administration of bromocriptine resulted in increased wakefulness and reduced slow-wave sleep (SWS) and rapid eye movement sleep (REM) during the 0- to 36-hour period. Reduction of SWS or REM during this time period was not followed by a rebound of SWS or REM during the next 36- to 84-hour period. In addition, there was a significant reduction of SWS during the entire 0- to 84-hour period. Administration of DHET to rats did not significantly affect sleep although there was a tendency for wakefulness to increase and for SWS and REM to decrease. It appears that the effects of repeated administration of the two ergot compounds on the sleep-wakefulness cycle in rats may be indicative of the drugs' role in fulfillment of sleep 'need'.

Animals↗
PubMed1980

Elimination of REM sleep rebound in rats by alpha-adrenoreceptor blockers, phentolamine and phenoxybenzamine.

Two alpha-adrenoreceptor blocking agents, phentolamine (5 mg/kg, IP) and phenoxybenzamine (10 mg/kg IP) were administered to rats deprived of rapid eye movement (REM) sleep for 24 hours to test the hypothesis that reduced noradrenergic transmission may abolish REM sleep rebound. The hypothesis was based on results from our previous studies which showed that administration to rats of diethyldithiocarbamate (DDC), a dopamine beta hydroxylase inhibitor, decreased the concentration of brain norepinephrine and reduced REM sleep permanently without the subsequent appearance of REM sleep rebound. Present results show that administration of both alpha-adrenoreceptor blockers abolished REM sleep rebound. At the time of maximum reduction of REM sleep, the concentration of 3-methoxy-4-hydroxyphenylethyleneglycol sulfate (MOPEGSO4), a final product of norepinephrine metabolism in the brain, was found increased in the whole brains of rats suggesting that the selected doses of the drugs were sufficient to produce effective central alpha-adrenergic receptor blockade. These data indicate that the action of both alpha-adrenoreceptor blocking agents in noradrenergic system was paralleled by the permanent loss of REM sleep and support the hypothesis implicating reduced noradrenergic transmission in elimination of REM sleep rebound.

Animals↗
PubMed1979

Hypnotic effect of tryptophan analog in rats.

The effects of DL 2-amino-3-(1-naphthyl) propanoic acid, a tryptophan analog, on sleep and brain chemistry were investigated in rats. Similar to previous findings with tryptophan, the tryptophan analog (30 mg/kg, IP) reduced slow-wave sleep (SWS) latency. The reduction in SWS latency occurred at a time when 5-hydroxytryptamine (5-HT) concentration was reduced in the cortex, pons-medulla and striatum-thalamus with no change in the concentration of 5-hydroxyindoleacetic acid, a major metabolite of 5-HT. At the same time, norepinephrine concentration was reduced in the cortex, hippocampus and striatum-thalamus with a marked reduction (40%) in cortical dopamine (DA). The reduction of cortical DA coincided with a 53% decrease in homovanillic acid, a major metabolite of DA. The behavioral effect of tryptophan analog for six hours, as monitored by the EEG, was an increase in SWS by 25 min and a decrease in waking by 29 min. These data suggest that the effects of the tryptophan analog on sleep may be due to the attenuation of the activity of brain catecholamines and imply that tryptophan may as well produce its hypnotic effect via a similar mechanism.

Animals↗
PubMed1979

Effects of diazepam on sleep, temperature, 5-hydroxyindoleacetic and homovanillic acids in cisternal cerebrospinal fluid of cats.

The effects of diazepam (DZ) (0.3--1.5 mg/kg, i.p.) on sleep, cisternal cerebrospinal fluid (CSF) concentrations of 5-hydroxyindoleacetic acid (5-HIAA) and homovanillic acid (HVA), and rectal temperature of cats were examined. The results showed that administration of DZ produced a significant increase (p = 0.02) in slow-wave sleep (SWS) with a peak occurring at a dose of 0.9 mg/kg. Further increase in doses of DZ decreased SWS. DZ administration produced no change in paradoxical sleep, rectal temperature, 5-HIAA or HVA CSF levels. Lack of correlation between various doses of DZ, and 5-HIAA or HVA concentrations in the presence of an increased percentage of SWS suggests a possible mode of DZ action mediated through a mechanism independent of monoamines. Usually monoamines are associated with normal sleep.

Animals↗
PubMed1978

Effects of cholinomimetic agents on pentobarbital anesthesia in mice.

We evaluated the effects of physostigmine, choline chloride, and neostigmine on pentobarbital anesthesia in mice, both when given before and after the administration of pentobarbital. Neostigmine and choline chloride had no effects. Physostigmine shortened the onset of pentobarbital anesthesia when given before pentobarbital but had no effects on the duration of anesthesia. However, when given after pentobarbital it shortened the duration of pentobarbital anesthesia. It seems unlikely that the above effects of physostigmine are dependent on the cholinergic system in the nervous system since neostigmine and choline chloride were without action. However, they may be due to the effects of physostigmine on the blood brain barrier permeability to pentobarbital.

Anesthetics↗
PubMed1976

Monoamine changes in the brain of cats during slow-wave sleep.

We have found that the metabolism of 5-hydroxytryptamine increases in the hippocampus and that the metabolism of dopamine decreases in the striatum and thalamus during slow-wave sleep, and we suggest that these changes are related to this stage of sleep. We have also found that the concentration of dopamine increases in the hippocampus during slow-wave sleep, and suggest that this may be related to the subsequent appearance of paradoxical sleep. These data raise new questions on the hippocampal role in the sleep-wakefulness cycle.

Animals↗