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Pierre-hervé Luppi - One of the best experts on this subject based on the ideXlab platform.

  • Illustration of the role of the DPGi in the network generating the sleep-waking cycle.
    2014
    Co-Authors: Olivier Clement, Patrice Fort, Sara Valencia Garcia, Paul-antoine Libourel, Sébastien Arthaud, Pierre-hervé Luppi
    Abstract:

    During waking, the adrenergic/noradrenergic groups (A/NA) are active. They tonically inhibit the DPGi GABAergic and the posterior hypothalamic GABA/MCH PS-on neurons as well as the SWS-active GABAergic neurons of the VLPO (ventrolateral preoptic Nucleus). They are also exciting the GABAergic PS-off neurons localized in the ventrolateral periaqueductal gray and the dorsal part of the deep mesencephalic Nucleus (vlPAG/dDpMe) in charge of the inhibition of the sublaterodorsal tegmental (SLD) PS-on glutamatergic neurons. The other wake-active (hypocretin, histaminergic, serotoninergic) and W/PS (cholinergic) active systems are activated and excite the thalamocortical system. During SWS, the VLPO GABAergic neurons are activated and inhibit all wake-active neurons. The DPGi GABAergic neurons are slightly active and contribute to the inhibition of the A/NA neurons from all groups. The onset and maintenance of PS is due to the activation of three GABAergic PS-on neurons localized in the posterior hypothalamus, the vlPAG/dDpMe and the DPGi. Each of these systems is responsible for the inhibition of one or several populations of wake-active neurons and of the PS-off GABAergic neurons localized in the vlPAG/dDpMe. The role of the DPGi GABAergic neurons is to specifically inactivate during PS the A/NA neurons from all groups. The disinhibited SLD PS-on glutamatergic neurons generate cortical activation by their projections to the thalamus and muscle atonia by means of their descending projection to GABA/glycinergic neurons localized in the ventral Gigantocellular Reticular Nucleus (GiV). These neurons hyperpolarize all somatic motoneurons.

  • Noradrenergic and adrenergic neurons strongly express c-FOS after muscimol inhibition of the DPGi.
    2014
    Co-Authors: Olivier Clement, Patrice Fort, Sara Valencia Garcia, Paul-antoine Libourel, Sébastien Arthaud, Pierre-hervé Luppi
    Abstract:

    Double-immunostained sections with TH (brown cytoplasmic staining) and c-FOS (black nuclear staining) at the level of A6 (A,D), A5 (B,E) and A1/C1 (C,F) noradrenergic cell groups after NaCl (top panel) or muscimol (bottom panel) injection in the DPGi. Black arrows point out double labeled neurons whereas black arrowheads and double arrowheads indicate TH singly and c-FOS singly labeled neurons, respectively. Scale bars, 50 µm for low power and 200 µm for high power photomicrographs in B, C, E and F. Abbreviations: 4V, 4th ventricle; A1/C1, A1 noradrenergic and C1 adrenergic groups; A5, A5 noradrenergic group; Gi, Gigantocellular Reticular Nucleus; IO, inferior olive; PnC, pontine Reticular Nucleus, caudal part; py, pyramidal tract; sp5, spinal trigeminal tract; Sp5O, spinal trigeminal Nucleus, oral part.

  • Numbers (mean ± SEM) of single CTb and double-labelled Fos/CTb neurons in 40 brain areas after injection of CTb in the LPGi in the PS-control (PSC), PS-deprived (PSD) and PS-recovery (PSR) conditions.
    2013
    Co-Authors: Chrystelle Sirieix, Damien Gervasoni, Pierre-hervé Luppi, Lucienne Léger
    Abstract:

    Legend of Table 3. The values displayed are an average, across 4 animals in each condition, of the sum of the neurons counted at 600 µm intervals through the full extent of each Nucleus. hello P≤0.05 ; hellohellohello P≤0.001 vs PSC ; # P≤0.05 ; ### P≤0.001 vs PSD. Abbreviations: A5: A5 noradrenergic area; antPAG: anterior periaqueductal gray; Au: auditory cortex; BST: bed Nucleus of the stria terminalis; CeM: central amygdaloid Nucleus; DA: dorsal hypothalamic area; DM: dorsomedial hypothalamic Nucleus; DMPAG: dorsomedial periaqueductal gray; DLPAG: dorsolateral periaqueductal gray; DPGi: dorsal paraGigantocellular Nucleus; DpMe: deep mesencephalic Nucleus; Ect: ectorhinal cortex; Gi: Gigantocellular Reticular Nucleus; GI: insular cortex; GiA: Gigantocellular Reticular Nucleus, alpha part; GiV: Gigantocellular Reticular Nucleus, ventral part; Irt: intermediate Reticular Nucleus; KF: Kölliker-Fuse Nucleus; LH: lateral hypothalamic area; LPAG: lateral periaqueductal gray; LPB: lateral parabrachial Nucleus; LPGi: lateral paraGigantocellular Nucleus; M1: primary motor cortex; MPB: medial parabrachial Nucleus; MVe: medial vestibular Nucleus; Pa: paraventricular hypothalamic Nucleus; PCRt: parvicellular Reticular Nucleus; PeF: perifornical Nucleus; PH: posterior hypothalamic Nucleus; PnC: pontine Reticular Nucleus, caudal part; PnO: pontine Reticular Nucleus, oral part; PnV: pontine Reticular Nucleus, ventral part; RMg: raphe magnus Nucleus; RPa: raphe pallidus Nucleus; ROb: raphe obscurus Nucleus; S1: primary somatosensory cortex; SLD: sublaterodorsal Nucleus; Sol: Nucleus of the solitary tract; vlPAG: ventrolateral periaqueductal gray; ZI: zona incerta.

  • Number (mean ± SEM) of single-CTb and double Fos/CTb neurons after CTb injection in the facial Nucleus. Counts were made in 3 rats during PS recovery following a 72h PS-deprivation.
    2013
    Co-Authors: Chrystelle Sirieix, Damien Gervasoni, Pierre-hervé Luppi, Lucienne Léger
    Abstract:

    Abbreviations: Gi : Gigantocellular Reticular Nucleus; GiA : Gigantocellular Reticular Nucleus, alpha part; GiV : Gigantocellular Reticular Nucleus, ventral part; Irt : intermediate Reticular Nucleus; LPGi : lateral paraGigantocellular Nucleus; PCRt : parvocellular Reticular Nucleus; RMg : raphe magnus Nucleus.

  • Distribution of the single CTb (black dots) and double-labelled Fos/CTb (red dots) in a PS-recovery rat after an injection of CTb in the facial Nucleus (Blackened area at -11.50).
    2013
    Co-Authors: Chrystelle Sirieix, Damien Gervasoni, Pierre-hervé Luppi, Lucienne Léger
    Abstract:

    Figures refer to the distance from the Bregma. Abbreviations : Gi, Gigantocellular Reticular Nucleus; GiV, Gigantocellular Reticular Nucleus, ventral part; IRt, intermediate Reticular Nucleus; PCRt, parvicellular Reticular Nucleus.

Lucienne Léger - One of the best experts on this subject based on the ideXlab platform.

Takeshi Kaneko - One of the best experts on this subject based on the ideXlab platform.

  • distribution of gabaergic and glycinergic premotor neurons projecting to the facial and hypoglossal nuclei in the rat
    The Journal of Comparative Neurology, 1997
    Co-Authors: Masahiko Takada, Takeshi Kaneko, Noboru Mizuno
    Abstract:

    The distribution of inhibitory premotor neurons for the facial and hypoglossal nuclei was examined in the lower brainstem of the rat. A retrograde axonal tracing method with the fluorescent tracer, tetramethylrhodamine dextran amine (TMR-DA), was combined with immunofluorescence histochemistry for glutamic acid decarboxylase (GAD), i.e., the enzyme involved in gamma-aminobutyric acid synthesis, or glycine. In the rats injected with TMR-DA unilaterally into the facial or hypoglossal Nucleus, the distribution of TMR-DA-labeled neurons showing GAD-like immunoreactivity (GAD/TMR-DA neurons) was essentially the same as that of TMR-DA-labeled neurons displaying glycine-like immunoreactivity (Gly/TMR-DA neurons). The distributions of GAD/TMR-DA and Gly/TMR-DA neurons in the rats injected with TMR-DA into the facial Nucleus were also similar to those in the rats injected with TMR-DA into the hypoglossal Nucleus. These neurons were seen most frequently in the lateral aspect of the pontine Reticular formation, the supratrigeminal region, the dorsal aspect of the lateral Reticular formation of the medulla oblongata, and the Reticular regions around the raphe magnus Nucleus and the Gigantocellular Reticular Nucleus pars alpha, bilaterally with a slight dominance on the side ipsilateral to the injection site. A number of GAD/TMR-DA and Gly/TMR-DA neurons were also seen in the oral and interpolar subnuclei of the spinal trigeminal Nucleus, bilaterally with a slight ipsilateral dominance. In the rats injected with TMR-DA into the facial Nucleus, GAD/TMR-DA and Gly/TMR-DA neurons were also encountered in the paralemniscal zone of the midbrain tegmentum bilaterally with an apparent dominance on the side contralateral to the injection site. A large part of these inhibitory premotor neurons for the facial and hypoglossal nuclei and the excitatory ones may constitute premotor neuron pools common to the orofacial motor nuclei implicated in the control of integrated orofacial movements. J. Comp. Neurol. 378:283–294, 1997. © 1997 Wiley-Liss, Inc.

  • gabaergic and glycinergic neurons projecting to the trigeminal motor Nucleus a double labeling study in the rat
    The Journal of Comparative Neurology, 1996
    Co-Authors: Masahiko Takada, Takeshi Kaneko
    Abstract:

    The distribution of GABAergic and glycinergic premotor neurons projecting to the trigeminal motor Nucleus (Vm) was examined in the lower brainstem of the rat by a double labeling method combining retrograde axonal tracing with immunofluorescence histochemistry. After injection of the fluorescent retrograde tracer, tetramethylrhodamine dextran amine (TRDA), into the Vm unilaterally, neurons labeled with TRDA were seen ipsilaterally in the mesencephalic trigeminal Nucleus, and bilaterally in the parabrachial region, the supratrigeminal and intertrigeminal regions, the Reticular formation just medial to the Vm, the principal sensory and spinal trigeminal nuclei, the pontine and medullary Reticular formation, especially the parvicellular part of the medullary Reticular formation, the alpha part of the Gigantocellular Reticular Nucleus, and the medullary raphe nuclei. Some of these neurons labeled with TRDA were found to display glutamic acid decarboxylase (the enzyme involved in GABA synthesis)-like or glycine-like immunoreactivity. Such double-labeled neurons were seen mainly in the supratrigeminal region, the Reticular region adjacent to the medial border of the Vm, and the dorsal part of the lateral Reticular formation of the medulla oblongata; a number of them were further scattered in the intertrigeminal region, the alpha part of the Gigantocellular Reticular Nucleus, the Nucleus raphe magnus, the principal sensory trigeminal Nucleus, and the interpolar subNucleus of the spinal trigeminal Nucleus. These neurons were considered to be inhibitory (GABAergic or glycinergic) neurons sending their axons to motoneurons in the Vm, or to local interneurons within and around the Vm.

  • premotor neurons for trigeminal motor Nucleus neurons innervating the jaw closing and jaw opening muscles differential distribution in the lower brainstem of the rat
    The Journal of Comparative Neurology, 1995
    Co-Authors: Takeshi Kaneko
    Abstract:

    The distribution of premotor neurons for trigeminal motor Nucleus neurons innervating the jaw-closing and jaw-opening muscles was examined in the lower brainstem of the rat by using retrograde and anterograde labeling techniques. First, Fluorogold, a fluorescent retrograde tracer, was injected into the dorsolateral or ventromedial division of the trigeminal motor Nucleus, each of which contains motoneurons innervating the jaw-closing or jaw-opening muscles, respectively. Second, Phaseolus vulgaris-leucoagglutinin, an anterograde tracer, was injected into each of the lower brainstem sites, where clusters of retrogradely labeled premotor neurons had been seen in the first set of experiments. Third, after injection of the anterograde tracer into a lower brainstem site, followed by injection of the retrograde tracer cholera toxin B subunit into a masticatory muscle, termination of anterogradely labeled axons onto retrogradely labeled motoneurons was confirmed with the aid of a confocal laser-scanning microscope. It was found that the premotor neurons distributed in the mesencephalic trigeminal Nucleus, medial part of the parabrachial region, supratrigeminal region, and dorsal parts of the principal sensory, oral spinal and interpolar spinal trigeminal nuclei project preferentially to the dorsolateral division of the trigeminal motor Nucleus, whereas those in the lateral part of the parabrachial region, intermediate parts of the principal sensory, oral spinal and interpolar spinal trigeminal nuclei, and alpha part of the Gigantocellular Reticular Nucleus project preferentially to the ventromedial division of the trigeminal motor Nucleus. The dorsal and lateral parts of the medullary Reticular formation and the medullary raphe nuclei contain premotor neurons of both types. Group k motoneurons, a cluster of trigeminal motoneurons that innervate the tensor tympani muscle, receive projection fibers predominantly from the dorsolateral part of the oral pontine Reticular formation.

  • immunohistochemical localization of substance p receptor in the central nervous system of the adult rat
    The Journal of Comparative Neurology, 1994
    Co-Authors: Yoshifumi Nakaya, Takeshi Kaneko, Ryuichi Shigemoto, Shigetada Nakanishi, Noboru Mizuno
    Abstract:

    In an attempt to reveal the function sites of substance P (SP) in the central nervous system (CNS), the distribution of SP receptor (SPR) was immunocytochemically investigated in adult rat and compared with that of SP-positive fibers. SPR-like immunoreactivity (LI) was mostly localized to neuronal cell bodies and dendrites. Neurons with intense SPR-LI were distributed densely in the cortical amygdaloid Nucleus, hilus of the dentate gyrus, locus ceruleus, rostral half of the ambiguus Nucleus, and intermediolateral Nucleus of the thoracic cord; moderately in the caudatoputamen, Nucleus accumbens, olfactory tubercle, median, pontine, and magnus raphe nuclei, laminae I and III of the caudal subNucleus of the spinal trigeminal Nucleus, and lamina I of the spinal cord; and sparsely in the cerebral cortex, basal Nucleus of Meynert, claustrum, Gigantocellular Reticular Nucleus, and lobules IX and X of the cerebellar vermis. Neurons with weak to moderate SPR-LI were distributed more widely throughout the CNS. The regional patterns of distribution of SPR-LI were not necessarily the same as those of SP-positive fibers. The entopedunucular Nucleus, substantia nigra, and lateral part of the interpeduncular Nucleus showed intense SP-LI but displayed almost no SPR-LI. Conversely, the hilus of the dentate gyrus, anterodorsal thalamic Nucleus, central Nucleus of the inferior colliculus, and dorsal tegmental Nucleus showed intense to moderate SPR-LI but contained few axons with SP-LI. These findings confirmed the presence of the "mismatch" problem between SP and SPR localizations. However, the distribution of SPR-LI was quite consistent with that of the SP-binding activity, which has been studied via autoradiography. This indicates that the sites of SPR-LI revealed in the present study represent most, if not all, sites of SP-binding activity.

Damien Gervasoni - One of the best experts on this subject based on the ideXlab platform.

Patrice Fort - One of the best experts on this subject based on the ideXlab platform.

  • Noradrenergic and adrenergic neurons strongly express c-FOS after muscimol inhibition of the DPGi.
    2014
    Co-Authors: Olivier Clement, Patrice Fort, Sara Valencia Garcia, Paul-antoine Libourel, Sébastien Arthaud, Pierre-hervé Luppi
    Abstract:

    Double-immunostained sections with TH (brown cytoplasmic staining) and c-FOS (black nuclear staining) at the level of A6 (A,D), A5 (B,E) and A1/C1 (C,F) noradrenergic cell groups after NaCl (top panel) or muscimol (bottom panel) injection in the DPGi. Black arrows point out double labeled neurons whereas black arrowheads and double arrowheads indicate TH singly and c-FOS singly labeled neurons, respectively. Scale bars, 50 µm for low power and 200 µm for high power photomicrographs in B, C, E and F. Abbreviations: 4V, 4th ventricle; A1/C1, A1 noradrenergic and C1 adrenergic groups; A5, A5 noradrenergic group; Gi, Gigantocellular Reticular Nucleus; IO, inferior olive; PnC, pontine Reticular Nucleus, caudal part; py, pyramidal tract; sp5, spinal trigeminal tract; Sp5O, spinal trigeminal Nucleus, oral part.

  • Illustration of the role of the DPGi in the network generating the sleep-waking cycle.
    2014
    Co-Authors: Olivier Clement, Patrice Fort, Sara Valencia Garcia, Paul-antoine Libourel, Sébastien Arthaud, Pierre-hervé Luppi
    Abstract:

    During waking, the adrenergic/noradrenergic groups (A/NA) are active. They tonically inhibit the DPGi GABAergic and the posterior hypothalamic GABA/MCH PS-on neurons as well as the SWS-active GABAergic neurons of the VLPO (ventrolateral preoptic Nucleus). They are also exciting the GABAergic PS-off neurons localized in the ventrolateral periaqueductal gray and the dorsal part of the deep mesencephalic Nucleus (vlPAG/dDpMe) in charge of the inhibition of the sublaterodorsal tegmental (SLD) PS-on glutamatergic neurons. The other wake-active (hypocretin, histaminergic, serotoninergic) and W/PS (cholinergic) active systems are activated and excite the thalamocortical system. During SWS, the VLPO GABAergic neurons are activated and inhibit all wake-active neurons. The DPGi GABAergic neurons are slightly active and contribute to the inhibition of the A/NA neurons from all groups. The onset and maintenance of PS is due to the activation of three GABAergic PS-on neurons localized in the posterior hypothalamus, the vlPAG/dDpMe and the DPGi. Each of these systems is responsible for the inhibition of one or several populations of wake-active neurons and of the PS-off GABAergic neurons localized in the vlPAG/dDpMe. The role of the DPGi GABAergic neurons is to specifically inactivate during PS the A/NA neurons from all groups. The disinhibited SLD PS-on glutamatergic neurons generate cortical activation by their projections to the thalamus and muscle atonia by means of their descending projection to GABA/glycinergic neurons localized in the ventral Gigantocellular Reticular Nucleus (GiV). These neurons hyperpolarize all somatic motoneurons.

  • The neuronal network responsible for paradoxical sleep and its dysfunctions causing narcolepsy and rapid eye movement (REM) behavior disorder
    Sleep Medicine Reviews, 2010
    Co-Authors: Pierre-hervé Luppi, Christelle Peyron, Damien Gervasoni, Emilie Sapin, Denise Salvert, Lucienne Léger, Olivier Clement, Patrice Fort
    Abstract:

    Summary Rapid eye movement (REM) sleep behavior disorder (RBD) is a parasomnia characterized by the loss of muscle atonia during paradoxical (REM) sleep (PS). Conversely, cataplexy, one of the key symptoms of narcolepsy, is a striking sudden episode of muscle weakness triggered by emotions during wakefulness, and comparable to REM sleep atonia. The neuronal dysfunctions responsible for RBD and cataplexy are not known. In the present review, we present the most recent results on the neuronal network responsible for PS. Based on these results, we propose an updated integrated model of the mechanisms responsible for PS and explore different hypotheses explaining RBD and cataplexy. We propose that RBD is due to a specific degeneration of a sub-population of PS-on glutamatergic neurons specifically responsible of muscle atonia, localized in the caudal pontine sublaterodorsal tegmental Nucleus (SLD). Another possibility is the occurrence in RBD patients of a specific lesion of the glycinergic/GABAergic pre-motoneurons localized in the medullary ventral Gigantocellular Reticular Nucleus. Conversely, cataplexy in narcoleptics would be due to the activation during waking of the caudal PS-on SLD neurons responsible for muscle atonia. A phasic glutamatergic excitatory pathway from the central amygdala to the SLD PS-on neurons activated during emotion would induce such activation. In normal conditions, the glutamate excitation would be blocked by the simultaneous excitation by the hypocretins of the PS-off GABAergic neurons localized in the ventrolateral periaqueductal gray and the adjacent deep mesencephalic Reticular Nucleus, gating the activation of the PS-on SLD neurons.

  • Paradoxical (REM) sleep genesis: the switch from an aminergic-cholinergic to a GABAergic-glutamatergic hypothesis.
    Journal of Physiology - Paris, 2006
    Co-Authors: Pierre-hervé Luppi, Christelle Peyron, Damien Gervasoni, Denise Salvert, Lucienne Léger, Laure Verret, Romain Goutagny, Patrice Fort
    Abstract:

    In the middle of the last century, Michel Jouvet discovered paradoxical sleep (PS), a sleep phase paradoxically characterized by cortical activation and rapid eye movements and a muscle atonia. Soon after, he showed that it was still present in "pontine cats" in which all structures rostral to the brainstem have been removed. Later on, it was demonstrated that the pontine peri-locus coeruleus alpha (peri-LCalpha in cats, corresponding to the sublaterodorsal Nucleus, SLD, in rats) is responsible for PS onset. It was then proposed that the onset and maintenance of PS is due to a reciprocal inhibitory interaction between neurons presumably cholinergic specifically active during PS localized in this region and monoaminergic neurons. In the last decade, we have tested this hypothesis with our model of head-restrained rats and functional neuroanatomical studies. Our results confirmed that the SLD in rats contains the neurons responsible for the onset and maintenance of PS. They further indicate that (1) these neurons are non-cholinergic possibly glutamatergic neurons, (2) they directly project to the glycinergic premotoneurons localized in the medullary ventral Gigantocellular Reticular Nucleus (GiV), (3) the main neurotransmitter responsible for their inhibition during waking (W) and slow wave sleep (SWS) is GABA rather than monoamines, (4) they are constantly and tonically excited by glutamate and (5) the GABAergic neurons responsible for their tonic inhibition during W and SWS are localized in the deep mesencephalic Reticular Nucleus (DPMe). We also showed that the tonic inhibition of locus coeruleus (LC) noradrenergic and dorsal raphe (DRN) serotonergic neurons during sleep is due to a tonic GABAergic inhibition by neurons localized in the dorsal paraGigantocellular Reticular Nucleus (DPGi) and the ventrolateral periaqueductal gray (vlPAG). We propose that these GABAergic neurons also inhibit the GABAergic neurons of the DPMe at the onset and during PS and are therefore responsible for the onset and maintenance of PS.