Biomedical subjects

R Cespuglio

Publications and source records attributed to R Cespuglio.

At least 19 recordsLinked to original sources

PubMed1991

Effects induced by the electrical stimulation of the nucleus raphe dorsalis upon hypothalamic release of 5-hydroxyindole compounds and sleep parameters in the rat.

Electrical stimulation (30 min; pulse 0.5 ms, 150 microA, 20 Hz) of the antero-dorsal part of the nucleus raphe dorsalis (n.RD) induces in the basal hypothalamus (n. arcuate and surrounding areas) a large axonal release of 5-hydroxyindole compounds (5-OHLes; about +300%) measured by means of voltammetric technique. During such a release, evidence for a direct detection of serotonin (5-HT) is reported. The above stimulation induces also marked aversive behaviors together with prolonged polygraphic arousal. Three hours later, a significant paradoxical sleep (PS) rebound occurs. Both the 5-OHLes release and the PS rebound observed after n.RD stimulation are suppressed by a p-chlorophenylalanine (PCPA) pretreatment of the animals. The 5-HT-hypnogenic factor dependence of the PS rebound observed after n.RD stimulation is discussed.

Animals↗

PubMed1991

Distribution of the pro-opiomelanocortin-immunoreactive axons in relation to the serotoninergic neurons in the dorsal raphe nucleus of the rat.

The anatomical relationships between pro-opiomelanocortin-containing axons and serotonin neurons in the nucleus raphe dorsalis (NRD) of the rat were examined at the light microscope level with antibodies against CLIP (corticotropin-like intermediate lobe peptide), alpha-MSH (alpha-melanocyte-stimulating hormone) and serotonin. Sequential double labeling was performed with either immunofluorescence or peroxidase-antiperoxidase techniques. It was observed that the network of POMC-immunoreactive axons displayed a gradient of decreasing density from rostral to caudal levels and from dorsal to ventral parts or the NRD. The examples of close proximity between immunoreactive axons and serotonin cell bodies or dendrites were rather scarce. On the whole, the immunoreactive fibers seemed to run quasi-independently of the serotonin neurons.

Adrenocorticotropic Hormone↗

PubMed1991

Immobilisation stress induces a paradoxical sleep rebound in rat.

An immobilisation stress (IS) of 2 h applied to rats at the beginning of the dark period (12 h), i.e. when the animals are more active, induces during the 10 consecutive h a significant rebound (+92%) of paradoxical sleep (PS) while slow-wave sleep state (SWS) is poorly affected. Two h of sleep deprivation, also applied at the beginning of the dark period and realized either by the platform technique or by maintaining the animals awake with gentle handling, do not affect significantly subsequent SWS and PS. Finally, when repetitive IS are inflicted to the animals (one IS of 2 h every 3 days) an attenuation of the PS rebound is observed. These data suggest that a qualitative aspect of the waking state as in an intense stressful situation might be the source of a hormonal process inducing a PS excess.

Animals↗

PubMed1991

Detection of the release of 5-hydroxyindole compounds in the hypothalamus and the n. raphe dorsalis throughout the sleep-waking cycle and during stressful situations in the rat: a polygraphic and voltammetric approach.

In the present work, voltammetric method combined with polygraphic recordings were used in animals under long-term chronic conditions; the extracellular concentrations of 5-hydroxyindole compounds (5-OHles) and in particular 5-hydroxyindoleacetic acid (5-HIAA) were measured in the hypothalamus and in the nucleus Raphe Dorsalis (n.RD). The hypothesis that extracellular detection of 5-HIAA, in animals under physiological conditions, might reflect serotonin (5-HT) release is suggested by the following observations: serotoninergic neurons are reported to contain only monoamine oxidase type B (MAO-B);--an inhibitor of such an enzyme, MDL 72145 (1 mg/kg), fails to decrease the extracellular 5-HIAA peak 3 height:--MAO type A is contained in non-5-HT cells or neurons;--only the inhibitor of this last type of enzyme (Clorgyline 2.5 mg/kg) induces a complete disappearance of the voltammetric signal. The 5-HIAA measured in the extracellular space thus comes from the 5-HT released and metabolized outside the 5-HT neurons. Throughout the sleep-waking cycle, 5-OHles release occurs following two different modes: 1--during sleep, in the vicinity of the 5-HT cellular bodies in the n.RD; this release might come from dendrites and be responsible for the 5-HT neuronal inhibition occurring during sleep; 2--during waking, at the level of the axonal nerve endings impinging on the hypothalamus; this release might be related to the synthesis of "hypnogenic factors". Finally, we have observed that in the hypothalamus, 30 min. of immobilization-stress (IS) induces a larger increase of the voltammetric signal (+80%) than a painful stimulation of the same duration (+30%); the possible link between the 5-OHles release occurring in this area during an IS and the subsequent paradoxical sleep rebound is discussed.

Allylamine↗

PubMed1990

Time-course variations induced by pargyline on the 5-hydroxyindole compounds measured in the nucleus raphe dorsalis and in blood: a voltammetric and HPLC approach in the rat.

Ninety min after pargyline (Pargy, 75 mg/kg) injection, the +300 mV voltammetric signal, measured in the nucleus raphe dorsalis (nRD) of freely moving rats, disappeared completely. This effect was also followed (2-7 h post-injection) by the reappearance of a peak (post-Pargy-peak) at the same +300 mV potential. The height of this post-Pargy signal was still decreased by Pargy (30 or 75 mg/kg). Endogenous 5-hydroxyindoleacetic acid (5-HIAA) contents, measured with HPLC in the nRD of Pargy-treated rats, exhibited analogous variations. Inhibition of monoamine oxidases by Pargy seems thus to be effective in blocking 5-HIAA production over only 2 h. The 15-fold increase of 5-HT endogenous content in the nRD (3 h after injection) was not reflected in the voltammetric extracellular measurements performed 90 min to 7 h after Pargy injection; this increase is suspected to be mainly intracellular.

Animals↗

PubMed1990

Circadian rest-activity rhythms in the anophthalmic, monocular and binocular ZRDCT/An mice. Retinal and serotoninergic (raphe) influences.

In the present study, two strains of mice were used: the control C57 Black/6 and the experimental ZRDCT/An, composed of anophthalmic (AN), monocular (mono) and binocular (bi) animals. The circadian rest-activity rhythms of these mice, submitted to a 12 h/12 h light/dark (L/D) cycle, present different characteristics. In C57 Black/6 animals the rhythms are classically synchronized to the L/D cycle with a maximal activity during the dark period, mainly at its beginning. In the AN mice, without exception, the rhythms are free running. In the bi and mono animals they are either synchronized to the L/D cycle, or synchronized but phase shifted in comparison with C57 Black/6, or free running. For the mono and bi animals, the typical or atypical mode of synchronization of their rhythms to the L/D cycle appears to be correlated with the ganglion cell density. It is well known that such a retinal component ensures the retino-hypothalamic connections. In the C57 Black/6 and AN mice, differential pulse voltammetric measurements of 5-hydroxyindoleacetic acid (5-HIAA, peak 3) extracellular concentrations have been also realized together with polygraphic recordings of the sleep/waking cycle. In both strains, the height of the 5-HIAA peak 3 recorded in the cortex is always the highest during active waking, and decreases during slow wave sleep and paradoxical sleep. Further, a circadian variation of this signal is superimposed to that of the waking state amount. Such circadian variations are synchronized to the L/D cycle in C57 Black/6 animals and free running in the AN mice.

Animals↗

PubMed1990

Voltammetric detection of the release of 5-hydroxyindole compounds throughout the sleep-waking cycle of the rat.

In the present work, differential pulse voltammetry (DPV) measurements of the extracellular fraction of 5-hydroxyindole compounds were performed in rats under long-term chronic conditions. In the nucleus Raphe Dorsalis (n.RD), the voltammetric signal measured at +300 mv (peak 3) disappeared completely 70 to 90 min after injection of Clorgyline (10 mg/kg), a monoamine oxidase inhibitor type A (MAOI-A); the signal measured in such conditions is thus dependent upon extracellular 5-hydroxyindoleacetic acid (5-HIAA peak 3). Deprenyl, an MAOI type B, at the same dose, induced only a slight increase in peak 3 height; according to the fact that MAO-B is selectively located in the 5-HT neurons and since their inhibition does not decrease 5-HIAA peak 3 nor the endogenous 5-HIAA content as measured with High Performance Liquid Chromatography (HPLC), 5-HIAA measured with DPV in the extracellular fluid of untreated animals might come from 5-HT released and metabolized by MAO-A outside the 5-HT neurons. In animals implanted for measurements of both voltammetric and polygraphic parameters, the 5-HIAA peak 3 measured mainly in the anterior and ventral part of the n.RD exhibited large increases in its height during slow-wave sleep (SWS: +39%) and paradoxical sleep (PS = +71%) as compared to the waking state (W = 100%); these variations could reflect the dendritic release of 5-HT. In the Caudate nucleus (n.Cd) the same voltammetric signal presented reverse fluctuations, i.e. an increase during W and a decrease during SWS and PS.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗

PubMed1990

Proopiomelanocortin (POMC)-derived peptides and sleep in the rat. Part 1--Hypnogenic properties of ACTH derivatives.

The sleep-wake effects of the proopiomelanocortin (POMC)-derived peptides, i.c.v. injected, are reported. Adrenocorticotropic hormone (ACTH, 1 microgram) induces an awakening effect, while its two derivatives, desacetyl-alpha-MSH (des-alpha-MSH, 1ng) and corticotropin-like intermediate lobe peptide (CLIP, 10 ng), are respectively able to increase slow wave sleep (SWS) and paradoxical sleep (PS); the hypnogenic effect of CLIP is also observed in hypophysectomized rats. Furthermore, two hypothalamic factors known to be involved in the control of POMC derivatives were also injected; MSH inhibiting Factor (MIF) does not influence the vigilance states, while Corticotropin Releasing Factor (CRF, 1 microgram) increases the waking state. Finally, some preliminary results, obtained with a restraint stress and suggesting a possible interrelation between stress, sleep and POMC derivatives, are discussed.

Adrenocorticotropic Hormone↗

PubMed1990

Proopiomelanocortin (POMC)-derived peptides and sleep in the rat. Part 2--Aminergic regulatory processes.

Apomorphine (Apo), a D1/D2 Dopamine (DA) agonist, at high doses (500 micrograms/kg) induces a short-lasting insomnia, antagonized by a secondary injection of corticotropin-like intermediate lobe peptide (CLIP, 10 ng); these effects are also observed with hypophysectomized (hypoX) rats. The administration of the serotonin (5-HT) agonist 8-hydroxy-2-di-n-propylamino-tetralin (8-OHDPAT, 0.3 mg/kg) induces also an insomnia which, unlike Apo, is followed by a significant PS rebound. CLIP, again, antagonizes the 8-OHDPAT-induced insomnia. Finally, Bromocriptine (5 mg/kg), an agonist for both DA and 5-HT, induces first an insomnia (antagonized by CLIP), followed by a PS rebound; these effects persist in hypoX rats.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

PubMed1989

[Role of hypothalamic adenosinergic systems in regulating states of wakefulness in the rat].

Immunohistochemical localization of adenosine deaminase (ADA), marker for the putative neurotransmitter/neuromodulator adenosine, has revealed a population of ADA-positive neurons in the ventrolateral hypothalamus in the rat brain. These posterior neurons possess adenosine uptake sites. We have studied the effects of local injections of adenosinergic drugs on the sleep-wake cycle in the rat. Microinjection of erythro-9-(hydroxy-2, nonyl-3) adenine (EHNA), a specific inhibitor of adenosine deaminase, resulted in a significant decrease in wakefulness (W) and an increase in deep slow wave sleep (SWS, or S2) and paradoxical sleep (SP). On the other hand, microinjections of soluflazine, a nucleoside transport inhibitor, increased W and decreased total sleep. These opposite modifications may reflect opposite variations in the extracellular concentrations of Ado and consequently different responses of A1/A2 adenosine receptors.

Adenine↗

PubMed1988

[Opposite variations of extracellular concentrations of 5-hydroxyindoleacetic acid (5-HIAA) measured by voltammetry of axonal terminals and cell bodies of the dorsal raphe nucleus through the sleep-wake cycle].

Differential pulse voltammetry was used for 5-hydroxyindoleacetic acid (5-HIAA) detection in the rat caudate (n. Cd) and Raphe Dorsalis (n. RD) nuclei, in chronic experimental conditions. In the anterior and ventral part of n. RD, large increases in the extracellular concentrations of 5-HIAA were reported during slow wave sleep (SWS) and paradoxical sleep (PS) whereas a decrease occurred during waking. These variations could reflect the dendritic release of serotonin. In n. Cd, opposite variations of the extracellular concentrations of 5-HIAA were observed i.e. increase during waking state and decrease during SWS and PS.

Animals↗

PubMed1986

Differential pulse voltammetry in vivo with working carbon fiber electrodes: 5-hydroxyindole compounds or uric acid detection?

Differential pulse voltammetry was performed in rats chronically implanted with carbon fiber electrodes in the caudate (n.Cd) and raphe dorsalis (n.RD) nuclei. The electrochemical signal obtained at the +300 mV potential (peak 3) in animals implanted for more than one week (long term chronic conditions, greater than 7 days) could be dependent upon the extracellular fraction of 5-hydroxyindolacetic acid (5-HIAA) since a single injection of Pargyline is sufficient to suppress it in n.Cd and n.RD. This result was obtained despite the tendency of Pargyline to increase n.Cd and n.RD endogenous concentrations of Uric Acid (UA) measured by High Performance Liquid Chromatography (HPLC). In contrast, in animals implanted for less than one week (short term chronic conditions, less than 7 days) peak 3 recorded in the same structure could be dependent upon extracellular fractions of 5-HIAA and UA since consecutive injections of Pargyline and Allopurinol are necessary to suppress this signal. The source of extracellular UA measured in brain by voltammetry, in such short term chronic conditions, might result from surgical trauma.

Animals↗

PubMed1985

Influence of proopiomelanocortin-derived peptides on the sleep-waking cycle of the rat.

The effects of i.c.v. injections of different proopiomelanocortin-derived peptides were tested on the rat sleep-waking cycle: adrenocorticotropic hormone (ACTH) had no effect. In contrast, administration of two ACTH-derived peptides was followed by a selective and significant increase of each sleep state: desacetyl-alpha-melanocyte-stimulating hormone induced an increase of slow-wave sleep, while corticotropin-like intermediate lobe peptide was followed by an increase of paradoxical sleep. Both alpha-melanocyte-stimulating hormone in its acetylated form and alpha-endorphin were inactive.

Adrenocorticotropic Hormone↗

PubMed1985

Factors influencing the properties of voltammetric carbon fibre electrodes: the importance of the pH of the medium used for the electrical treatment and of the resin coating of the fibres.

Electrical treatment of resin-coated voltammetric carbon fibre electrodes with triangular voltage at low (1.1) pH resulted in electrodes almost insensitive to ascorbic acid (AA) and dihydroxyphenylacetic acid (DOPAC) while their response to 5-hydroxyindoleacetic acid (5-HIAA) was practically the same as after treatment in the usually employed pH 7.4 medium. Electrodes treated at high pH (12.0), on the other hand, were more sensitive to AA and DOPAC than those treated at pH 7.4 and less sensitive to 5-HIAA. Exposing resin-coated electrodes to the treatment media without electrical treatment was not sufficient to obtain the same results as with the application of the current. Electrodes without resin coating were sensitive to AA without electrical treatment while coated electrodes were not. Electrical treatment increased the sensitivity of non-coated electrodes and rendered coated electrodes even more sensitive than non-coated ones. Treatment of coated electrodes for a maximum sensitivity to 5-HIAA was found to require less time than to obtain maximum sensitivity to the other compounds. Present results suggest that it is possible to prepare selective voltammetric electrodes by choosing the right parameters for their electrical pretreatment.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1985

[Differential pulse voltammetry: focus on the measurement of 5-hydroxyindole compounds and uric acid in the brain].

The electrochemical signal obtained at the +300 mV potential (peak 3) in rats implanted for more than one week could be dependent upon extracellular fraction of 5-hydroxyindolacetic acid (5-HIAA) since a single injection of Pargyline is sufficient to suppress it in caudate and raphe dorsalis nuclei. In contrast, in rats implanted for less than one week, this signal could be dependent upon extracellular fractions of 5-HIAA and uric acid since consecutive injections of Pargyline and Allopurinol are necessary to suppress it.

Animals↗

PubMed1985

[Hypnogenic effects of des-acetyl-alpha-MSH and CLIP (ACTH 18-39) in the rat].

In the rat, the intraventricular administration of ACTH (adrenocorticotropic hormone) has no effect upon the sleep-waking cycle. However, administration of two ACTH-derived peptides is followed by a selective and significant increase of each sleep state: Des-alpha-MSH (Des-acetyl-alpha-melanocyte stimulating hormone) administration induces an increase of slow wave sleep, while CLIP (corticotropin-like intermediate lobe peptide) is followed by an increase of paradoxical sleep.

Adrenocorticotropic Hormone↗

PubMed1983

Temperature-dependent variations of 5-hydroxyindoles in ventricular cerebrospinal fluid--an in vivo voltammetric study.

The in vivo voltammetric signal of 5-OH-indoles increased or decreased in the ventricular cerebrospinal fluid when body temperature was artificially increased or decreased in rats in acute experiments. The increase of the signal occurring after raising the body temperature was facilitated by premedication with the monoamine oxidase inhibitor pargyline. It was not abolished by pretreatment with the serotonin synthesis inhibitor para-chlorophenylalanine, although the latter caused an 85% decrease of ventricular 5-OH-indole level. No similar effects were demonstrable in the 5-OH-indole signal of the caudate nucleus recorded simultaneously. An increase of the 5-OH-indole peak was found also in animals chronically implanted with voltammetric electrodes when the ambient temperature was increased in their cages. According to the results of in vitro experiments, a direct physical effect of changes in brain temperature on the sensitivity of the voltammetric electrodes cannot account for changes found in the cerebrospinal fluid. These data, therefore, demonstrate that the increase of body temperature is followed by an increase of 5-OH-indole concentration in the ventricular cerebrospinal fluid. The in vivo voltammetric technique appears to be a suitable method for studying the serotonergic mechanisms involved in thermoregulatory processes.

Animals↗

PubMed1983

Voltammetric measurements of 5-hydroxyindole compounds in the suprachiasmatic nuclei: circadian fluctuations.

This study concerns the voltammetric signal appearing at a +300 mV potential (peak 3) recorded from the suprachiasmatic nuclei (SCN) of rats under acute and chronic conditions. In acute conditions, and in order to accurately localize the working electrode, a topographical study of the peak 3 height was first realized in the frontal plane containing the SCN by use of differential pulse voltammetry and monocarbon fiber electrodes. In the same conditions, the effects of clorgyline and reserpine were studied. Clorgyline decreased peak 3 while reserpine increased it. Contrary to 5-HT, 5-HIAA contents of the SCN, measured with high performance liquid chromatography, demonstrate analogous variations. All these data suggest that it is essentially 5-HIAA which is responsible for peak 3 from the SCN. In unanesthetized, freely moving rats, under a 12/12 h light-dark cycle, spontaneous and circadian variations of the SCN's peak 3 were studied, during the rest-activity cycle. Multifiber working electrodes were used for this purpose. During spontaneous and successive periods of rest and activity peak 3 height was always found to be higher during activity. Further, these spontaneous variations were superimposed with a circadian variation exhibiting its acrophasis during the dark period. Our data suggest that the release and catabolism of serotonin is greater in waking than in sleeping animals. They also suggest, that the rostral raphe system, phase locked with the SCN, plays an important role in the circadian variations measured.

5-Hydroxytryptophan↗