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J L Valatx

Publications and source records attributed to J L Valatx.

At least 19 recordsLinked to original sources
PubMed1992

[Demonstration of prolactin messenger RNA after amplification in the brain in rats].

By means of immunocytochemistry, a central neuronal network containing a prolactin-like substance has been described in the rat. In order to demonstrate the synthesis of this peptide in these cells, we examined the presence of prolactin messenger RNA (PRL mRNA) in several brain samples including the pituitary gland. Amplification of the PRL mRNA was performed by the polymerase chain reaction technique, followed by southern blotting and hybridization with a specific oligonucleotide. Results showed the presence of the expected cDNA (468 bp) in the hypothalamus. Another cDNA with a lower molecular weight was also observed.

Animals↗
PubMed1990

[Sleep: current data in 1990].

Relations between serotonin and sleep have been re-evaluated in the waking and sleep periods. During sleep serotonin-containing neurons cease to function, as do all monoaminergic neurons. During waking one of the roles played by serotonin is to stimulate the synthesis of hypnogenic peptides. At the same time, serotonin inhibits paradoxical sleep as its occurrence during waking would be dangerous. In addition, under the influence of certain peptides serotonin, released by the dendrites of median raphe neurons, exerts a self-inhibition on their activity at the onset of sleep. The number of hypnogenic peptides discovered is ever increasing, raising the problem of their specificity and mode of action within the spontaneous sleep-waking cycle. Recent studies have reappraised the mechanisms of recovery after sleep deprivation. It is now believed that recovery is modulated by the intensity of stress during waking and not by the duration of waking, hence the hypnogenic role played by hormones, such as ACTH derivatives, that are involved in stress. Even more recent studies on the relationship between the mechanisms of sleep and those of central temperature are leading to a number of questions likely to modify the current hypotheses concerning sleep.

Histamine↗
PubMed1989

[Prolactin-secreting neurons in the dorsolateral hypothalamus in Sprague-Dawley rats].

By means of immunocytochemical techniques ovine prolactin like immunoreactivity (oPRL-LIR) has been demonstrated in the perikarya located around fornix in the dorso-lateral part of the rat hypothalamus. No PRL-LIR was observed in the arcuate n. perikarya. Immunoreactive fibers were present in the hypothalamus, medial thalamus, accumbens and amygdaloid nuclei.

Amygdala↗
PubMed1988

Hypophysectomy in monosodium glutamate-pretreated rats suppresses paradoxical sleep rebound.

Control untreated and pretreated female rats at birth with 10 injections of monosodium glutamate (MSG, 4 mg/g b. wt.) were hypophysectomized (HYPX) at 45-60 days of age and their sleep-waking cycle continuously registered. In control rats, hypophysectomy was followed by a 35.7% decrease in paradoxical sleep (PS) duration while it has no effect on the sleep of MSG-treated rats. After 24 h of PS deprivation, there was a normal immediate rebound of PS in the control HYPX and MSG rats while there was no significant rebound in the HYPX-MSG-treated rats. It is concluded that neuropeptides from arcuate nucleus and hypophysis are involved in a PS rebound mechanism.

Animals↗
PubMed1988

Effects of hypophysectomy on the sleep of neonatally monosodium glutamate-treated rats.

Monosodium Glutamate (MSG), known to induce neuronal cell degeneration of the arcuate nucleus of the hypothalamus, was subcutaneously injected (4 mg/g body wt.) at postnatal days 1 to 5 or 1 to 10 in female rats. Hypophysectomy was performed at 45-60 days of age. Sleep parameters were continuously recorded for at least 7 days. Results indicated that hypophysectomized (HYPX) NaCl-treated rats showed an increase of Slow Wave Sleep (SWS) (+29.6%) and a decrease of Paradoxical Sleep (PS) (-36.7%) durations. In MSG-treated rats, hypophysectomy did not alter SWS durations but it increased PS durations as MSG dosing increased. It was concluded that arcuate nucleus neurons seemed to be not critically involved in sleep production mechanisms.

Aging↗
PubMed1988

[Circadian rhythms of slow-wave sleep and paradoxical sleep are in opposite phase in genetically hypoprolactinemic rats].

In eleven genetically hypoprolactinemic rats (IPL nude rats) and five control rats (OFA), the sleep-waking cycle was continuously registered for 14 days at two ambient temperatures. At 23 degrees C, the slow wave sleep (SWS) duration of IPL rats was significantly higher (+6.8%, t = 5.4, p less than 0.001) than that of control rats, while the paradoxical sleep (PS) duration was lowered by 31.8% (t = 9.4, p less than 0.001). The circadian rhythm of PS disappeared while that of SWS persisted unchanged. At 30 degrees C, both sleep durations reached the level of control rats. The circadian rhythm of PS was however completely reversed: the PS acrophase was at 01 h while that of SWS was at 12 hrs. This first observation of spontaneous dissociation of the two states of sleep supports the hypothesis of two distinct circadian clocks, one for SWS, another for PS. It is suggested that hypothalamic prolactin and/or other still unknown genetic alterations might be responsible for the observed change in the PS circadian rhythm.

Animals↗
PubMed1987

[Absence of paradoxical sleep rebound in hypophysectomized rats pretreated at birth with sodium glutamate].

Control untreated female rats and rats pretreated at birth with ten injections of monosodium glutamate (MSG; 4 mg/g b.w.) were hypophysectomized (Hypox) at 45-60 days of age and their sleep-waking cycle continuously registered. After 24 hrs. of PS deprivation, there was an immediate increase of PS (rebound) in the control Hypox and MSG rats while there was no increase in Hypox-MSG rats. Factors from arcuate nucleus and/or from the hypophysis are probably involved in the mechanisms of PS rebound.

Animals↗
PubMed1986

Neonatal monosodium glutamate dosing alters the sleep-wake cycle of the mature rat.

Alterations of the sleep-wake cycle have been studied in male adult rats after neonatal administration of monosodium glutamate (MSG; 4 X 4 mg/g body wt.). Results indicated that MSG treatment caused: an almost complete disappearance of ACTH and alpha-MSH immunoreactive (IR) perikarya in the rostral part of the arcuate nucleus; an increase in total sleep duration with a more pronounced effect on paradoxical sleep. Regarding circadian rhythmicity there was a trend to a decomposition of the 24 h period into ultradian components (12 h, 8 h, 6 h harmonics). The participation of pro-opiomelanocortin peptides in sleep regulation is discussed.

Activity Cycles↗
PubMed1985

Effects of hypothalamic paraventricular lesions on sleep in rats.

In 7 rats 45-86% of the hypothalamic paraventricular tissue was destroyed by electrolytic coagulations. During the first 6 post-operative days the mean daily amount of paradoxical sleep was significantly decreased, and the circadian sleep-walking cycles of paradoxical and slow-wave sleep were abolished. The slow-wave sleep rhythm then became normal, but in paradoxical sleep the acrophase was shifted, and in one animal the rhythm was completely inversed. Thus the hypothalamic paraventricular nucleus seems to play a modulating role in the production of paradoxical sleep and in the generation of its rhythm.

Animals↗
PubMed1979

Strain differences in amphetamine sensitivity in mice. I. A diallel analysis of open field activity.

Experiments are reported which show that 1 mg/kg of d-methylamphetamine HCl induced hyperactivity in pigmented strains (C57BR, C57BL/6, and SEC) and hypoactivity or no change in albino strains (BALB/c, A, and AKR) of mice. In F1 hybrids, the B6 genotype was partially dominant over BR and C, and BR over C. In animals back-crossed to C parents widespread distributions with two peaks were obtained in control experiments, and amphetamine induced hyperactivity in 38% of the albino population, and hypoactivity or no significant change in 45% of the pigmented one. This genetic study indicates that genes influencing locomotor activity are independent from those influencing amphetamine sensitivity. From results obtained in back-crosses and C57BL/6-c2J mice, the albino gene does not seem to be involved in the hypoactive effect of amphetamine.

Animals↗
PubMed1979

Strain differences in amphetamine sensitivity in mice. II. Overcompensation of paradoxical sleep after deprivation in two C57 strains.

d-Methylamphetamine (1--4 mg/kg) induced wakefulness for 3--5 h followed by paradoxical sleep (PS) rebound in C57BR, C57BL/6, and BALB/c mice. Slow-wave sleep (SWS) and PS suppression time were proportional to the given dose and different among strains. It was also dependent on the time of injection. Later PS rebound was significant in C57 strains, and in certain cases greater than PS loss, whereas rebound was small in BALB/c mice and PS loss was not completely compensated.

Animals↗
PubMed1977

[Phasic activity in rats].

At the central level, in the rat, phasic activity has been recorded during paradoxical sleep and in acute conditions after injection of reserpine or parachlorophenylalanine. At the external level, during paradoxical sleep, the extraocular muscles lateral rectus, superior rectus and superior oblique are activated in both plastic and tonic manners. The muscles of the whiskers are also activated; these muscular activations are more often than not synchronous with the eye movements (80%). The time distribution of these ocular movements is homogenous. Reserpine induces phasic muscular activations of the extraocular muscles.

Animals↗
PubMed1976

[Y-maze learning in two strains of mice. Effects of instrumental and pharmacologic sleep deprivation].

Effects of instrumental and pharmacological deprivation of sleep on Y-maze learning have been studied in two inbred strains of mice (C57BR/cd/Orl and C57BL/6/Orl), having identical sleep rhythms, but mainly differing in their ability to learn. Administration of alpha-methyl-DOPA (100 mg/kg) provokes complete suppression of paradoxical sleep (PS) for 9-11 h. Injection immediately after each training session over the first 5 days caused a delay in acquisition of an active avoidance task in C57BR mice. Treated C57BL/6 mice exhibited a significant facilitation of acquisition. Similar results were obtained by instrumental deprivation of sleep for 10 h.

Animals↗
PubMed1975

[Action of alpha-methyl-dopa on waking-sleep cycles in two inbred strains of mice, C57BR and C57BL/6 (author's transl)].

The effects of alpha-methyl-Dopa at several dose levels on waking-sleep cycle of 175 mice from two inbred strains (C57BR and C57BL/6) have been studied. The results showed that each dose (25, 50, 100, 200 and 400 mg/kg), of alpha-methyl-Dopa completely suppresses paradoxical sleep (PS), after a period of sedation. Duration of PS inhibition varied as a function of dose, time of injection, and strain of mice. Using a multiple injection schedule of one injection per day for 5 consecutive days, there was suppression of nocturnal PS followed at the 4th day by rebound during day light hours.

Animals↗