Biomedical subjects

M Jouvet

Publications and source records attributed to M Jouvet.

At least 109 records · Page 6Linked to original sources

PubMed1991

Daily variations in concentration of vasoactive intestinal polypeptide immunoreactivity in discrete brain areas of the rat.

The concentration of VIP-like immunoreactivity (VIP-LI) was determined by radioimmunoassay at various times of the day in 11 discrete brain areas and in the antehypophysis of rats maintained on a regular 12 h/12 h light-dark cycle. In the suprachiasmatic and periventricular nuclei the VIP-LI increased during the dark period and decreased during the subsequent light period. In addition, the VIP-LI exhibited complex variations in the locus coeruleus, the periaqueductal gray matter and the paraventricular nucleus, but did not change in the other areas investigated.

Analysis of Variance↗

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↗

PubMed1991

The role of 5-hydroxytryptophan (5-HTP) in the regulation of the sleep/wake cycle in parachlorophenylalanine (p-CPA) pretreated rat: a multiple approach study.

In the rat, the insomnia which follows the administration of parachlorophenylalanine (p-CPA), a serotonin synthesis inhibitor, is transiently reversed either by intra-cisternal injection of L-5-HTP or by an associated injection of 5-HTP and an L-aromatic-acid-decarboxylase inhibitor (benserazide). Histochemical, immunohistochemical and chemical investigations showed that 5-HTP administration does not lead to a detectable increase in cerebral 5-HT. These findings suggest that the restoration of sleep after p-CPA treatment could be mediated by the central action of 5-HTP.

5-Hydroxytryptophan↗

PubMed1991

The posterior hypothalamus is responsible for the increase of brain temperature during paradoxical sleep.

Electroencephalogram, caudate nucleus temperature (Tc), ear skin temperature (Te) as well as cerebral blood flow (CBF) measured by a thermal clearance method, were recorded simultaneously and continuously in cats. After baseline recording in which we confirmed the increase of Tc during paradoxical sleep (PS), neuronal cell bodies of the mesencephalic reticular formation and/or the posterior hypothalamus (PH) were destroyed with ibotenic acid. Only PH lesions were followed by either a suppression of the increase or even a decrease of Tc during PS while Te variations were not modified. The decrease in CBF, which was always associated with Tc increase, was suppressed after the PH lesion. These results led us to the conclusion that the increase of Tc at the onset of PS is due to a decrease in CBF. Furthermore, it may be hypothesized that the decrease in CBF depend upon an active vasoconstriction process originating in the PH.

Animals↗

PubMed1991

Distribution of type B monoamine oxidase immunoreactivity in the cat brain with reference to enzyme histochemistry.

We studied the detailed distributions and morphology of structures immunoreactive to type B monoamine oxidase, and compared them with those stained by monoamine oxidase enzyme histochemistry in the brain of cats treated with or without colchicine. By means of the indirect immunohistochemical method in conjunction with type B monoamine oxidase monoclonal antibody, we demonstrated type B monoamine oxidase immunoreactivity in neuronal cell bodies, fibers and astroglial cells in the cat brain. As expected, the distribution of type B monoamine oxidase-immunoreactive cell bodies overlapped that of serotonin-containing ones in the lower brainstem and midbrain, as well as that of histaminergic ones in the posterior hypothalamus. We found novel cell groups containing type B monoamine oxidase in the areas described below. Intense type B monoamine oxidase-immunopositive and enzymatically active neurons, corresponding to liquor-contact ones, were discovered in the wall of the central canal of the spinomedullary junction. Weak immunoreactivity was identified in neurons of the dorsal motor nucleus of the vagus, parvocellular reticular formation and locus coeruleus complex, which have been reported to contain type A monoamine oxidase enzymatic activity. Type B monoamine oxidase-immunostaining in these structures was enhanced by treatment with colchicine. In addition, lightly immunostained cells were distinguished in the caudal portion of the hypothalamic arcuate nucleus, area of tuber cinereum, retrochiasmatic area, and rostral portion of the paraventricular thalamic nucleus after colchicine treatment. These cells also displayed monoamine oxidase activity; however, it was difficult to enzymatically characterize their nature due to its weak activity and sensitivity to inhibitors of both A and B. Distinct type B monoamine oxidase-immunoreactive fibers and terminal-like dots were abundant in the whole brain, particularly in the central gray, dorsal pontine tegmentum, interpeduncular and pontine nuclei, nucleus of the solitary tract and dorsal motor nucleus of vagus, where dense innervations of serotonergic fibers have been reported. Their immunoreactive density increased after colchicine treatment, but monoamine oxidase enzymatic reaction did not. An intense immunoreactivity could be seen in many glial cells in parts of the brain including myelinated axon pathways. The densest accumulation of such labeled glial cells was found in the central gray, inferior olive, medial geniculate body, substantia nigra, ventral tegmental area of Tsai, retrorubral area, hypothalamus, thalamus and bed nucleus of the stria terminalis. In contrast, the striatum contained less numerous type B monoamine oxidase-immunoreactive and enzymatically active astroglial cells in comparison with the other structures.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1991

[Paradoxical sleep: is it the guardian of psychological individualism].

The brain is the sole organ of homeotherms that do not undergo cell division. We thus have to explain how certain aspects of psychological heredity (found in homozygotes twins raised in different surroundings) may persist for a whole life (psychological individuation). A definitive genetic programming during development (by neurogenesis) is unlikely due to the plasticity of the nervous system. That's why we have to consider the possibility of an iterative genetic programming. The internal mechanisms (synchronous) of paradoxical sleep (SP) are particularly adapted to such programming. This would activate an endogenous system of stimulation that would stimulate and stabilize receptors genetically programmed by DNA in some neuronal circuits. The excitation of these neurons during SP leads to oniric behaviours that could be experimentally revealed--the lists of these behaviours are specific to each individual and indirect data suggest a genetic component of this programming. Amongst the mechanisms allowing the iterative programming of SP, sleep is particularly important. Security--and hence the inhibition of the arousal system--is a sine qua non condition for genetic programming to take place. In that sense, sleep could very well be the guardian of dreaming. On the other hand, sleep seems to be necessary for the accumulation of energetic resources used by the cholinergic mechanisms of SP. The temporal modalities of SP (diachronic organization) are also discussed in relation to phylogenesis. Thus, the absence of SP in poikilotherms is explained by a continual neurogenesis in the adult. During ontogenesis in mammals, a stage of programming by neurogenesis (seismic sleep) precedes the appearance of SP so long as the programming system isn't functional. The presence, or absence, of rebound after SP deprivation is interpreted in terms of the existence, or non existence, of stress during SP suppression. An explanation is proposed to account for the absence of specific effects of SP deprivation in humans. In the same way somatic intraspecific variability is one of the conditions of evolution, it is proposed that one of the functions of SP is to maintain psychological variability in a given population.

Animals↗

PubMed1990

Aromatic L-amino acid decarboxylase-immunohistochemistry in the cat lower brainstem and midbrain.

By indirect immunohistochemistry, the present study examined the distribution of neuronal structures in the cat medulla oblongata, pons, and midbrain, showing immunoreactivity to aromatic L-amino acid decarboxylase (AADC), which catalyzes the conversion of L-3, 4-dihydroxyphenylalanine (L-DOPA) to dopamine, and 5-hydroxytryptophan to serotonin (5HT). With simultaneous and serial double immunostaining techniques, immunoreactivity to this enzyme was demonstrated in most of the catecholaminergic and serotonergic neurons. We could also demonstrate AADC-IR cell bodies that do not contain tyrosine hydroxylase (TH-) or 5HT-immunoreactivity (called "D-type cells") outside such monoaminergic cell systems. At the medullo-spinal junction, very small D-type cells were found within and beneath the ependymal layer of the 10th area of Rexed surrounding the central canal. D-type cells were localized in the caudal reticular formation, nucleus of the solitary tract, a dorsal aspect of the lateral parabrachial nucleus, and pretectal areas as have been reported in the rat. Furthermore, the present study describes, in the cat brainstem, new additional D-type cell groups that have not been reported in the rat. Dense or loose clusters of D-type cells were localized in the external edge of the laminar trigeminal nucleus, dorsal motor nucleus of the vagus, external cuneate nucleus, nucleus praepositus hypoglossi, central, pontine, and periaqueductal gray, superficial layer of the superior colliculus, and area medial to the retroflexus. D-type cells were loosely clustered in the lateral part of the central tegmental field dorsal to the substantia nigra, extending dorsally in the medial division of the posterior complex of the thalamus and medial side of the brachium of the inferior colliculus. They extended farther rostrodorsally along the medial side of the nucleus limitans and joined with the pretectal cell group. Almost all these cells were very small and ovoid to round with 1-2 short processes with the exception of dorsal motor vagal cells. AADC-IR axons were clearly identified in the vagal efferent nerves, longitudinal medullary pathway, dorsal tegmental bundle rostral to the locus coeruleus. Serotonergic axons were identified not only in the central tegmentum field and lateral side of the central superior nucleus, but also in the ventral surface of the medulla oblongata. We describe principal densely stained fiber plexuses in the cat brainstem. The findings of the present study provide a morphological basis for neurons that decarboxylate endogenous and exogenous L-DOPA, 5HTP, and other aromatic L-amino acids.

Animals↗

PubMed1990

Iontophoretic application of unconjugated cholera toxin B subunit (CTb) combined with immunohistochemistry of neurochemical substances: a method for transmitter identification of retrogradely labeled neurons.

In this report, we demonstrate that cholera-toxin B subunit (CTb) is a very sensitive retrograde tracer in the central nervous system when recognized by streptavidin-peroxidase immunohistochemistry. We further show that: (1) injection of a small volume of CTb gives rise to small sharply defined injection sites limited to the cell group of interest associated with the labeling of all the known afferent projections, (2) CTb is taken up, and anterogradely as well as retrogradely transported in damaged but not intact fibers of passage, (3) CTb can be applied iontophoretically, allowing us to study the afferents to small cell groups without any evidence of tissue necrosis in the sites and therefore without artefactual labeling due to uptake by damaged fibers of passage, (4) the use of 4% paraformaldehyde fixative ideally suited for the preservation of most neural antigens, the addition of a 48 h colchicine treatment and the development of a double immunohistochemical method allow the biochemical characterization of the cell of origin of particular pathways in the CNS, (5) CTb is also anterogradely transported with an extensive filling of axons and axon terminals and thereby opens up the possibility of identifying simultaneously the afferents as well as the efferents of the group of cells studied and finally (6) the very long conservation of the preparation, the possibility of counterstaining it and of making camera lucida drawings allow easy and precise localization of the retrogradely labeled cells.

Afferent Pathways↗

PubMed1990

Nuclei of origin of monoaminergic, peptidergic, and cholinergic afferents to the cat trigeminal motor nucleus: a double-labeling study with cholera-toxin as a retrograde tracer.

The aim of the present study was to determine the brainstem afferents and the location of neurons giving rise to monoaminergic, cholinergic, and peptidergic inputs to the cat trigeminal motor nucleus (TMN). This was done in colchicine treated animals by using a very sensitive double immunostaining technique with unconjugated cholera-toxin B subunit (CT) as a retrograde tracer. After CT injections in the TMN, retrogradely labeled neurons were most frequently seen bilaterally in the nuclei reticularis parvicellularis and dorsalis of the medulla oblongata, the alaminar spinal trigeminal nucleus (magnocellular division), and the adjacent pontine juxtatrigeminal region and in the ipsilateral mesencephalic trigeminal nucleus. We further observed that inputs to the TMN arise from the medial medullary reticular formation (the nuclei retricularis magnocellularis and gigantocellularis), the principal bilateral sensory trigeminal nucleus, and the dorsolateral pontine tegmentum. In addition, the present study demonstrated that the TMN received 1) serotonergic afferents, mainly from the nuclei raphe obscurus, pallidus, and dorsalis; 2) catecholaminergic afferent projections originating exclusively in the dorsolateral pontine tegmentum, including the Kölliker-Fuse, parabrachialis lateralis, and locus subcoeruleus nuclei; further, that 3) methionin-enkephalin-like inputs were located principally in the medial medullary reticular formation (nuclei reticularis magnocellularis and gigantocellularis and nucleus paragigantocellularis lateralis), in the caudal raphe nuclei (Rpa and Rob) and the dorsolateral pontine tegmentum; 4) substance P-like immunoreactive neurons projecting to the TMN were present in the caudal raphe and Edinger-Westphal nuclei; and 5) cholinergic afferents originated in the whole extent of the nuclei reticularis parvicellularis and dorsalis including an area located ventral to the nucleus of the solitary tract at the level of the obex. In the light of these anatomical data, the present report discusses the possible physiological involvement of TMN inputs in the generation of the trigeminal jaw-closer muscular atonia occurring during the periods of paradoxical sleep in the cat.

Afferent Pathways↗

PubMed1990

Inhibition by carbachol microinjections of presumptive cholinergic PGO-on neurons in freely moving cats.

The effects of microinjections of a cholinergic agonist, carbachol (0.2 micrograms/0.2 microliters), were examined on a population of presumptive cholinergic mesopontine PGO-on neurons that presents a tonic pattern of discharge during waking and exhibits short spike bursts preceding the onset of dorsal lateral geniculate PGO waves during paradoxical sleep and slow wave sleep just prior to it. PGO-on neurons were activated antidromically by the stimulation of the dorsal lateral geniculate, pulvinar and/or medial and intralaminar thalamic nuclei. They were all characterized by a long spike duration and a slow conduction velocity. Microinjections of carbachol near unit recording sites in freely moving cats induced a complete suppression of the spontaneous tonic activity during waking, but did not suppress the spontaneous phasic burst activity during sleep. Carbachol microinjections also resulted in a marked reduction in responsiveness of PGO-on neurons to orthodromic stimulation. These spike depressant effects lasted for approximately 90-120 min and were reversed completely by a local or systemic administration of atropine sulfate. These findings point to a direct inhibition of central cholinergic PGO-on neurons via a muscarinic autoreceptor and a difference in the mechanisms underlying the generation of tonic and phasic burst activity of PGO-on neurons occurring during waking and sleep.

Animals↗

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

Involvement of histaminergic neurons in arousal mechanisms demonstrated with H3-receptor ligands in the cat.

The effects of histamine H3-receptor ligands on sleep-waking parameters were studied in freely moving cats. Oral administration of (R)alpha-methylhistamine (alpha MHA), a H3-agonist, caused a significant increase in deep slow wave sleep while that of thioperamide, a H3-antagonist, enhanced wakefulness in a marked and dose-dependent manner. The arousal effects of thioperamide were prevented by pretreatment with alpha MHA or mepyramine, a H1-receptor antagonist. The findings support the hypothesis that the histaminergic neurons are critically involved in arousal mechanisms and suggest that H3-receptors play an active part in these mechanisms by regulating histamine transmission.

Animals↗

PubMed1990

Dopamine- and dopa-immunoreactive neurons in the cat forebrain with reference to tyrosine hydroxylase-immunohistochemistry.

The distribution of cell bodies containing immunoreactivities to dopamine (DA), L-3,4-dihydroxyphenylalanine (DOPA) and tyrosine hydroxylase (TH) was studied immunohistochemically in the cat forebrain especially in the hypothalamus with or without intraventricular administration of colchicine. In normal cats, DA-immunoreactive (IR) neurons, whose intensity of immunostainings was variable from one to another, were localized exclusively in the hypothalamus and showed a distribution pattern similar to that of TH-IR ones. They were distributed in the posterior, dorsal and periventricular hypothalamic areas. Arcuate cells showed no or very weak DA-immunoreactivity. Weak to intense DOPA-IR cells were distributed in a similar manner to DA-IR ones but were far smaller in number. In colchicine-treated animals, DA- and DOPA-immunoreactivities were enhanced particularly in arcuate and dorsal hypothalamic cells. A cluster composed of small DA- and DOPA-IR cells was identified in the area ventral to the mamillothalamic tract equivalent to rat A13c TH-IR cell group. Colchicine treatment enabled us to visualize a large number of TH-IR perikarya in the medial and lateral preoptic areas, anterior commissure nucleus, basal forebrain, area closely related to the organum vasculosum laminae terminalis, and some in the bed nucleus of the stria terminalis as has been reported in other species. However, virtually none of these cells contained detectable DA- and DOPA-immunoreactivities.

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

Responses of presumed cholinergic mesopontine tegmental neurons to carbachol microinjections in freely moving cats.

The effects of microinjections of a cholinergic agonist, carbachol (0.2 microgram/0.2 microliter), were examined on three different types of rostrally projecting tonic neurons that we have reported previously in the dorsal part of the pontomesencephalic tegmentum known to contain numerous cholinergic cell bodies: 1) tonic type I slow (Type I-S); 2) tonic type I rapid (Type I-R); and 3) tonic type II (Type II) (El Mansari et al. 1989). Microinjections of carbachol near unit recording sites in freely moving cats induced within a few minutes a complete suppression of the spontaneous activity and a marked reduction in orthodromic excitation of identified and non-identified type I-S neurons. These effect lasted for approximately 90-120 min and were reversed by local (0.4 microgram/0.2 microliter) or systemic (0.1-0.2 mg/kg, i.m.) administration of atropine sulfate. In contrast, the cholinergic agonist had no consistent effects on tonic type II nor on tonic type I-R neurons. In the light of these and other recent findings, we suggested the direct inhibition of central cholinergic neurons via muscarinic receptors, on the one hand, and the cholinergic nature of type I-S, but not type I-R nor type II neurons, on the other.

Action Potentials↗

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↗