Search PubMed⌕ Search

Biomedical subjects

R Cespuglio

Publications and source records attributed to R Cespuglio.

At least 73 records · Page 4Linked to original sources
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↗
PubMed1983

Differential pulse voltammetry in brain tissue: III. Mapping of the rat serotoninergic raphe nuclei by electrochemical detection of 5-HIAA.

Differential pulse voltammetry using a new type of carbon fiber electrode, electrochemically treated, is described. The working electrode contains 3 pyrolytic carbon fibers, and passes more current, thus giving a greater sensitivity (with the PRG5 Tacussel polarographic system) than the original monofiber electrodes. It is now possible to investigate brain areas where the monofiber electrodes, working near the limit of PRG5 sensitivity, showed too small a signal. These electrodes have, in addition, better mechanical resistance and can be used (after trypsin cleaning and further electrochemical treatment) for several experiments. Electrochemical measurements made in the nucleus raphe dorsalis before and after treatment with p-chlorophenylalanine, reserpine, clorgyline and clorgyline followed by reserpine, suggest that as in the striatum 5-hydroxyindoleacetic acid (5-HIAA) is mainly responsible for peak 3. The map of the raphe system made with this technique is well correlated with the serotoninergic system of the raphe: the highest peak heights are recorded in the raphe dorsalis.

Animals↗
PubMed1983

[Voltammetric detection of extracellular 5-hydroxyindole compounds at the level of cell bodies and the terminals of the raphe system: variations during the wake-sleep cycle in the rat in chronic experiments].

In rats, chronically implanted for measurements of both voltammetric and polygraphic parameters, variations of the electrochemical signal corresponding to extracellular 5-hydroxyindole compounds (peak 3) were measured during the sleep-waking cycle. The higher amplitude of this signal is always measured during waking. It decreases during slow-wave sleep (20 to 30%) and reaches its lower value during paradoxical sleep (30 to 40%). This phenomenon has been found in all structures investigated, cerebral cortex, caudate nuclei, dorsal hippocampus, suprachiasmatic nuclei, cerebellum, nuclei raphe dorsalis, centralis, pontis and magnus.

Animals↗
PubMed1982

Alterations in the sleep-waking cycle induced by cooling of the locus coeruleus area.

Bilateral or unilateral, localized and reversible cooling (+10 degrees C) of the anterior part of the locus coeruleus area (LCp) in the cat induced, in rapid succession, slow wave sleep (SWS) and a transitory phase of SWS + PGO. These states of sleep were followed in 40-50% of the animals by paradoxical sleep (PS). These effects (on SWS, SWS + PGO and PS) occurred following repetitive periods of short duration cooling and were maintained during long duration cooling (70 min). Unilateral cooling of the ventral part of the locus coeruleus area (LC alpha) and peri-LC alpha induced wakefulness, regardless of the states of sleep in which the cooling was performed. After a cryolesion (-24 degrees C) of the nucleus raphe dorsalis, cooling of the LCp did not induce a hypnogenic effect. Electrical stimulation of the locus coeruleus area, however, always induced wakefulness.

Animals↗
PubMed1981

[Hypnogenic properties of the vasoactive intestinal polypeptide in rats].

The intraventricular injection of 100 ng of vasoactive intestinal polypeptide (VIP) is followed by a significant increase of paradoxical sleep in the Rat. In P. chlorophenylalanine pretreated insomniac Rats which do not present spontaneous paradoxical sleep episodes, intraventricular injection of VIP induces normal quantities of this state of sleep.

Animals↗
PubMed1981

Differential pulse voltammetry in brain tissue. I. Detection of 5-hydroxyindoles in the rat striatum.

In vitro, differential pulse voltammetry combined with electrochemically treated carbon fiber electrodes enabled detection, in different solution of 5-hydroxyindole compounds, of an oxidation peak 3 at +300 mV. In vivo, a striatal peak 3 was also recorded at this potential. Electrolytic or 5,7-dihydroxytryptamine lesions interrupting the medial forebrain bundle (MFB) were followed by a decrease of 65% and 64% in peak height, but not elimination of the peak. Biochemical determinations were significantly correlated to the peak 3 measurements. The existence of peak 3 as well as hydroxyindole compounds in blood suggested a blood contamination under the experimental conditions employed. This possibility is confirmed both by the complete disappearance of striatal peak 3 in animals with the MFB lesioned and surgically prepared a week before recordings, and by biochemical measurements in parachlorophenylalanine-treated or perfused (phosphate-buffered saline solution) animals.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1981

Differential pulse voltammetry in brain tissue. II. Detection of 5-hydroxyindoleacetic acid in the rat striatum.

Differential pulse voltammetry with electrochemically treated carbon fiber electrodes was used to study, in anesthetized rats, the alterations of the striatal electrochemical signal appearing at +300 mV (peak 3), following pharmacological manipulation of the animals. Decreases in peak 3 were obtained after injections of NSD 1015, Ro 4-4602 and Clorgyline. This, in conjunction with biochemical measurements, suggested that 5-hydroxyindoleacetic acid (5-HIAA) is, to a considerable extent, responsible for this electrochemical signal. Increases in peak 3 obtained after reserpine, L-tryptophan and D,L-5-HTP, as well as biochemical data reinforced this hypothesis, as did the detection of peak 3 in cerebrospinal fluid and its increase after probenecid injection. The occurrence of a feed-back mechanism is discussed following injection of D,L-5-HTP.

5-Hydroxytryptophan↗
PubMed1981

Voltammetry in the striatum of chronic freely moving rats: detection of catechols and ascorbic acid.

Differential pulse voltammetry used in combination with an electrochemically treated carbon fiber electrode allowed to detect ascorbic acid (AA) and 3,4-dihydroxyphenylacetic acid (DOPAC) in the striatum of unanaesthetized freely moving rats. Carbon fiber electrodes were implanted under light halothane anaesthesia. When the rat recovered from anaesthesia, voltammograms were recorded every 2.5 min for about 5 h. During the last 3 h the signals corresponding to AA and DOPAC appeared stable and reproducible, allowing comparisons between control and pharmacological experiments. After the in vivo experiments, the electrodes were calibrated in AA and DOPAC solutions. Striatal AA and DOPAC levels were thus estimated to be 306 and 17.7 microM respectively. DOPAC signals were increased by haloperidol and chloral hydrate, decreased by amphetamine and suppressed by pargyline. In pargyline pretreated rats the catechol signal slightly re-appeared after amphetamine injections. This signal was attributed to dopamine (DA) and estimated to a concentration less than 50 nM DA. The AA current recorded in the striatum was not modified when dopaminergic terminals selectively degenerated. The AA signal was decreased by chloral hydrate or halothane anaesthesia and increased by amphetamine injections. This latter effect depended on the presence of dopaminergic terminals. This shows that the increasing current effect of amphetamine, previously observed by non-selective techniques, should be attributed to AA rather than DA. These results confirm that the catechol compound electrochemically detected in the striatum is the direct metabolite of the DA, i.e. DOPAC, and support the thesis of a functional relationship between AA levels and dopaminergic neurotransmission.

3,4-Dihydroxyphenylacetic Acid↗