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Biomedical subjects

G Arankowsky-Sandoval

Publications and source records attributed to G Arankowsky-Sandoval.

13 recordsLinked to original sources
PubMed2001

Sleep and memory deficits in the rat produced by experimental infection with Trypanosoma cruzi.

We investigated whether the infection with Trypanosoma cruzi in rats could produce functional alterations of the central nervous system. The experimental group received an injection of 150,000 trypomastigotes / rat, whereas the control group received a saline injection. Spontaneous alternation behavior (SAB) tests and sleep-wake cycle recordings were obtained at the end of the parasitaemia. Results showed that the infected animals had significant sleep impairments, as denoted by an increase in the number of wake periods and a reduction of rapid eye movement sleep amount. SAB performance was also found to be impaired in these animals, as compared to the control group. Our results suggest that the rat is a suitable model for brain dysfunction studies in Chagas' disease.

Animals↗
PubMed1999

Attenuation of morphine-induced behavioral changes in rodents by D- and L-glucose.

Administration of d-glucose enhances learning and memory in several tasks and also attenuates memory impairments and other behavioral effects of several drugs, including morphine. The present experiment compared the effects of peripherally administered d-glucose with those of l-glucose, a stereoisomer of d-glucose that is not metabolized and does not readily cross the blood-brain barrier. Like d-glucose, though at somewhat different doses, peripherally administered l-glucose attenuated morphine-induced deficits in spontaneous alternation performance in rats and mice and attenuated morphine-induced hyperactivity in mice. l-Glucose did not raise circulating levels of plasma d-glucose, suggesting that the effects of l-glucose are not secondary to increased availability of d-glucose. Using direct injections of d- and l-glucose and morphine into the medial septum of rats, the findings indicate that d-glucose but not l-glucose attenuated morphine-induced deficits in spontaneous alternation performance; indeed, intraseptal injections of l-glucose alone impaired spontaneous alternation performance. These findings suggest that peripheral l-glucose antagonizes morphine-induced behavioral effects by a peripheral signaling mechanism, one distinct from the mechanisms that mediate at least some of the effects of d-glucose on brain function.

Animals↗
PubMed1996

Prenatal exposure to alcohol in adult rats: relationships between sleep and memory deficits, and effects of glucose administration on memory.

Previous studies show that prenatal exposure to alcohol results in sleep deficits in rats, including reductions in paradoxical sleep. Little is known, however, about the extent or duration of sleep impairments beyond the neonatal period. The present experiment examined effects of prenatal exposure on sleep in young adulthood. Three-hour, daytime sleep EEGs were obtained in 6-month-old female rats prenatally exposed to alcohol. Compared to isocaloric pair-fed and ad libitum control groups, the alcohol-exposed group showed reduced paradoxical sleep. Non-paradoxical sleep did not differ between groups. Concurrent deficits were obtained in radial arm maze, but not inhibitory (passive) avoidance, performance. One year later, at the age of 18 months, alcohol-exposed rats showed deficits in spontaneous alternation behavior which were reversed by administration of glucose (100 mg/kg). Deficits in paradoxical sleep at 6 months of age were highly correlated with deficits in spontaneous alternation behavior at 18 months of age, in individual, alcohol-exposed animals. These results provide the first evidence that prenatal exposure to alcohol results in selective and persistent deficits in sleep. They also show that measures of paradoxical sleep can predict impaired memory over a large portion of the life span, and suggest that glucose can attenuate memory deficits in this population.

Acetaldehyde↗
PubMed1995

Morphine-induced deficits in sleep patterns: attenuation by glucose.

Morphine effects on many neural and behavioral measures, including tests of learning and memory, are attenuated by increased circulating glucose levels. Using systemic injections, we investigated the ability of glucose to attenuate sleep deficits induced by morphine administration in the rat. Morphine at 1 mg/kg produced a moderate decrease in slow wave sleep which was prevented by concomitant administration of 100 mg/kg of glucose. A higher dose of morphine (10 mg/kg) severely delayed the onset of both slow wave sleep and REM sleep. These delays were attenuated by concurrent administration of 250 mg/kg of glucose. Thus, glucose reversals of morphine effects are also extended to measures of sleep.

Animals↗
PubMed1994

Glucose attenuates the effect of combined muscarinic-nicotinic receptor blockade on spontaneous alternation.

Glucose administration reverses the effects of both muscarinic and nicotinic cholinergic receptor antagonists on memory and other measures. In experiment 1, we found that glucose attenuated impairments on spontaneous alternation after muscarinic (scopolamine, 0.5 mg/kg) or nicotinic (mecamylamine, 5.0 mg/kg) receptor blockade. In experiment 2, we examined whether glucose could reverse the spontaneous alternation impairments produced by combined muscarinic-nicotinic receptor blockade. Scopolamine (0.1 mg/kg) and mecamylamine (2.5 mg/kg) when administered separately did not modify alternation performance, but when coadministered they decreased spontaneous alternation scores. This decrease was attenuated by glucose at 100, 300, 500 and 3000 mg/kg. These findings suggest that glucose may attenuate the behavioral impairment by enhancing cholinergic activity and/or other neurotransmitter systems.

Animals↗
PubMed1992

Enhancement of REM sleep with auditory stimulation in young and old rats.

Auditory stimulation applied during rapid eye movement (REM) sleep enhances the duration of REM sleep in cats and humans. The present experiment investigated whether auditory stimulation would enhance REM sleep in young (3-6 months) rats, and also in old (22-24 months) rats which have impaired REM sleep. Baseline sleep records were obtained on two days. Sleep patterns were then assessed during auditory stimulation test sessions. In young rats, auditory stimulation was administered during each REM sleep bout. In old rats, auditory stimulation was administered on a fixed schedule (10 min of stimulation alternating with 15 min quiet). The day after the stimulation session, an additional sleep record (Day 2) was obtained for each rat. In young rats, auditory stimulation enhanced both REM sleep duration and total REM sleep time. In the old rats, which showed impaired sleep measures as compared to young animals, auditory stimulation enhanced both total REM sleep time and the number of REM sleep periods. Residual proactive effects of auditory stimulation (Day 2) were observed in both young and old rats. Thus, auditory stimulation is an effective manipulation with which to augment REM sleep in both young and old rats, and partially attenuates REM sleep impairments in old rats.

Acoustic Stimulation↗
PubMed1989

REM sleep enhancement induced by sensory stimulation is prevented by kainic acid lesion of the pontine reticular formation.

It has been shown that auditory or somatic stimulation during rapid eye movement (REM) sleep is capable of producing a significant increase in ponto-geniculo-occipital (PGO) spike density as well as in REM sleep duration. The purpose of this study was to determine the role of the medial pontine reticular formation (PRF) in mediating such increase of REM sleep duration. After a baseline recording whereby on the same recording day the control and the stimulus (auditory or somatic) alternated with each REM, a group of cats was lesioned with kainic acid in the PRF. The sleep-wake cycle was recorded again on days 15, 30 and 45 post-lesion, following the same procedure. The results showed no changes in REM sleep duration and PGO spike density in the lesioned animals. However, when sensory stimulation was applied it was ineffective in producing REM sleep enhancement, although it was able to increase PGO spike density. These findings suggest that the effects of sensory stimulation on REM sleep duration are accomplished through the PRF, probably by inducing an increase in the excitability levels of such neurons, and further suggests that PGO spike density and REM duration are independent of each other.

Acoustic Stimulation↗
PubMed1987

Rapid eye movement (REM) sleep and ponto-geniculo-occipital (PGO) spike density are increased by somatic stimulation.

It has been shown that REM sleep duration and ponto-geniculo-occipital (PGO) spike density can be enhanced by auditory stimulation. The purpose of this study was to determine whether this effect is restricted to the auditory sensory modality or whether somatic stimulation can produce similar effects. Cats implanted with electrodes for recording the sleep-wake cycle were additionally prepared with clip electrodes placed in the neck for somatic stimulation. Such stimulus was applied at the beginning and throughout each REM sleep period. The effect of this procedure was compared to a similar period when no stimulus was applied. The results showed that somatic stimulation induced a significant increase in REM duration (60.2%) and PGO spike density. Since the effects of somatic stimuli are identical to auditory ones, it is suggested that all sensory modalities may share the property of influencing the mechanisms which regulate the maintenance of REM sleep. Such mechanisms are discussed in terms of an increase in the excitability levels of polymodal medial reticular neurons.

Acoustic Stimulation↗
PubMed1986

Vasoactive intestinal polypeptide (VIP) and cerebrospinal fluid (CSF) of sleep-deprived cats restores REM sleep in insomniac recipients.

In the past few years a steadily increasing number of substances have been suggested to qualify as sleep-inducing factors. Most 'sleep factors' appear to exert their effects on slow-wave sleep. Recently, however, it has been shown that the cerebrospinal fluid (CSF) of sleep-deprived cats may contain a rapid eye movement (REM) sleep factor, and that vasoactive intestinal peptide (VIP) may be a specific REM sleep inducer. The purpose of this study is to determine whether the CSF of sleep-deprived cats and VIP can reverse insomnia produced by parachlorophenylalanine (PCPA). Donor cats were sleep-deprived for 24 h and their CSF extracted. Some donor cats were additionally pre-treated with chloramphenicol, and some extracted CSF was heated. Recipient cats were injected with 400 mg/kg i.p. of PCPA on two consecutive days. Twenty-four h after the second injection, the recipient cats were intraventricularly injected with a 100-microliters of the various CSF types or 200 ng of VIP. The results showed that only CSF from sleep-deprived cats and VIP were capable of restoring REM sleep in the otherwise PCPA insomniac cats. Since the return of REM sleep was through an increase in its frequency, it is suggested that the CSF of sleep-deprived cats contains a VIP-like sleep factor possibly involved in triggering REM sleep.

Animals↗
PubMed1986

Suprachiasmatic nucleus transplants function as an endogenous oscillator only in constant darkness.

Rats which sustained lesions of the suprachiasmatic nucleus (SCN) were transplanted with fetal hypothalamic tissue which included the SCN. After the graft, animals were kept under a 12:12 light-dark (LD) cycle during 6 weeks at which time half the animals were placed in constant light (LL) and half in constant darkness (DD). The results showed that all grafted rats recovered the photoperiod under LD, but under constant conditions rats began to free-run only in DD. The results suggest that the grafted tissue functions as a self-sustained oscillator only in darkness.

Animals↗
PubMed1986

Cholinergic reduction of REM sleep duration is reverted by auditory stimulation.

It was previously shown that an auditory stimulus given prior to and throughout a rapid eye movement (REM) sleep period was capable of inducing a significant increase in REM sleep duration and pontogeniculo-occipital (PGO) spike density. The purpose of this study was to determine whether the increase in REM duration is dependent on PGO spike density. We administered atropine to cats at doses of 0.1-0.6 mg/kg and the effects on REM duration and PGO spikes was determined. The doses of 0.2 and 0.3 mg/kg of atropine were then utilized to compare REM sleep periods with and without auditory stimulation. The results showed that both REM duration and PGO spikes were decreased by atropine, but could be dissociated from each other depending on the doses. In addition, it was shown that the auditory stimulus protected the animals from the effects of atropine but only in relation to REM sleep duration. The results indicate that both REM sleep duration and PGO spikes have a cholinergic component and that the auditory stimulus exerts its REM enhancing properties in a manner which seems to be independent of the PGO spike density. The results are discussed in terms of receptor availability and/or excitability levels of medial reticular neurons.

Acoustic Stimulation↗