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Rhumatologue

Docteur JACQUES GLOWINSKI

RPPS 10001353332
📊 Reconnaissance scientifique : 77/100📝 231 articles publiés📚 HAL (8)🎓 6 thèses dirigées

Diplômes

🎓 DES & spécialité ordinale

  • Rhumatologie (SM)

🎓 Diplômes

  • DE Docteur en médecine

Source : Annuaire Santé ANS (FHIR Practitioner.qualification) · Mises à jour quotidiennes.

Direction de thèses

🎓 6 thèses dirigées

Source theses.fr — signal de direction d'équipe / statut PU-PH (à confirmer via le site universitaire).

Activité de recherche & publications

Source : bases de données publiques (OpenAlex, PubMed).

h-index

77

h articles cités ≥ h fois chacun. Un h de 77 = 77 publications avec 77+ citations.

Citations

22 690

Publications

231

i10-index

170

Thématiques principales

  • Neuroscience and Neuropharmacology Research ×116
  • Neurotransmitter Receptor Influence on Behavior ×92
  • Receptor Mechanisms and Signaling ×65
  • Neuropeptides and Animal Physiology ×30
  • Ion channel regulation and function ×20
Voir sur OpenAlex ↗

Source : OpenAlex (CC0, OurResearch). Indicateurs académiques agrégés sur 250 M+ d'œuvres.

Bibliographie

Source : HAL — archive ouverte CCSD/CNRS (couvre articles, chapitres EMC, communications congrès, thèses).

Lieu de consultation

Tarifs & secteur de conventionnement

Secteur de conventionnement non disponible (médecin hospitalier ou non présent dans l'Annuaire santé CNAM des libéraux conventionnés).

📊 Comprendre le remboursement

Prendre rendez-vous & contact

🗓 Trouver sur Doctolib📇 Ajouter à mes contacts

Lien Doctolib = recherche Google site:doctolib.fr (le 1er résultat est presque toujours le profil correct s'il existe).

Articles de presse (1)

Source : Google News (recherche par nom complet — homonymes possibles, vérifier le contenu).

Top publications · les plus citées

  • 1
    Alpha1b-adrenergic receptors control locomotor and rewarding effects of psychostimulants and opiates

    The Journal of neuroscience : the official journal of the Society for Neuroscience · 2002

    📚 234 citations🎯 RCR 6.76Top 5% NIH🔓 Open Access📄 PDF gratuit ↗
    Lire l'abstract Crossref ↓

    Drugs of abuse, such as psychostimulants and opiates, are generally considered as exerting their locomotor and rewarding effects through an increased dopaminergic transmission in the nucleus accumbens. Noradrenergic transmission may also be implicated because most psychostimulants increase norepinephrine (NE) release, and numerous studies have indicated interactions between noradrenergic and dopaminergic neurons through α1-adrenergic receptors. However, analysis of the effects of psychostimulants after either destruction of noradrenergic neurons or pharmacological blockade of α1-adrenergic receptors led to conflicting results. Here we show that the locomotor hyperactivities induced byd-amphetamine (1–3 mg/kg), cocaine (5–20 mg/kg), or morphine (5–10 mg/kg) in mice lacking the α1b subtype of adrenergic receptors were dramatically decreased when compared with wild-type littermates. Moreover, behavioral sensitizations induced byd-amphetamine (1–2 mg/kg), cocaine (5–15 mg/kg), or morphine (7.5 mg/kg) were also decreased in knock-out mice when compared with wild-type. Ruling out a neurological deficit in knock-out mice, both strains reacted similarly to novelty, to intraperitoneal saline, or to the administration of scopolamine (1 mg/kg), an anti-muscarinic agent. Finally, rewarding properties could not be observed in knock-out mice in an oral preference test (cocaine and morphine) and conditioned place preference (morphine) paradigm.Because catecholamine tissue levels, autoradiography of D1 and D2 dopaminergic receptors, and of dopamine reuptake sites and locomotor response to a D1 agonist showed that basal dopaminergic transmission was similar in knock-out and wild-type mice, our data indicate a critical role of α1b-adrenergic receptors and noradrenergic transmission in the vulnerability to addiction.

  • 2
    Bidirectional activity-dependent plasticity at corticostriatal synapses

    The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005

    📚 188 citations🎯 RCR 3.82Top 12% NIH🔓 Open Access📄 PDF gratuit ↗
    Lire l'abstract Crossref ↓

    Corticostriatal projections originate from the entire cerebral cortex and provide the major source of glutamatergic inputs to the basal ganglia. Despite the importance of corticostriatal connections in sensorimotor learning and cognitive functions, plasticity forms at these synapses remain strongly debated. Using a corticostriatal slice preserving the connections between the somatosensory cortex and the target striatal cells, we report the induction of both non-Hebbian and Hebbian forms of long-term potentiation (LTP) and long-term depression (LTD) on striatal output neurons (SONs). LTP and LTD can be induced selectively by different stimulation patterns (high-frequency trains vs low-frequency pulses) and were evoked with similar efficiency in non-Hebbian and Hebbian modes. Combination of LTP–LTD and LTD–LTP sequences revealed that bidirectional plasticity occurs at the same SONs and provides efficient homeostatic mechanisms leading to a resetting of corticostriatal synapses avoiding synaptic saturation. The effect of temporal relationship between cortical stimulation and SON activity was assessed using spike-timing-dependent plasticity (STDP) protocols. An LTP was observed when an action potential was triggered in the striatal neuron before the cortical stimulus, and, conversely, an LTD was induced when the striatal neuron discharge was triggered after the cortical stimulation. Such STDP was reversed when compared with those described so far in other mammalian brain structures. This mechanism may be essential for the role of the striatum in learning of motor sequences in which sensory and motor events are associated in a precise time sequence.

  • 3
    Influence of the hippocampus on interneurons of the rat prefrontal cortex

    The European journal of neuroscience · 2004

    📚 159 citations🎯 RCR 3.63Top 12% NIH
    Lire l'abstract Crossref ↓

    AbstractThe hippocampus and prefrontal cortex (PFC), two structures implicated in learning and memory processes, are linked by a direct hippocampo‐prefrontal pathway. It has been shown that PFC pyramidal cells receive monosynaptic excitatory inputs from the hippocampus and, in this study, we sought to determine the influence of the hippocampus on PFC interneurons in anesthetized rats. Extracellular recordings were coupled to juxtacellular injections of neurobiotin or biotinylated dextran amine to morphologically differentiate interneurons from pyramidal cells. In all cases, the action potentials of labeled interneurons were of shorter duration (< 0.70 ms) than those of identified pyramidal cells (> 0.70 ms). Single pulse stimulation of the hippocampal CA1/subiculum region induced an excitatory response in 70% of recorded interneurons in the prelimbic and medial‐orbital areas of the PFC. In contrast to the one to two action potentials generated by pyramidal cells, an important group of interneurons fired a burst of action potentials in response to hippocampal stimulation. A large proportion of these excitatory responses was probably monosynaptic as their latency is consistent with the conduction time of the hippocampo‐prefrontal pathway. In addition, when both a pyramidal cell and an interneuron were simultaneously recorded and both responded to stimulation, the interneuron consistently fired before the pyramidal cell. In conclusion, the hippocampus exerts a direct excitatory influence on PFC interneurons and is thus capable of feedforward inhibition of pyramidal cells. Hippocampal output is spatially and temporally focalized via this inhibitory process and consequently could facilitate the synchronization of a specific subset of PFC neurons with hippocampal activity.

Publications scientifiques (49) — classées par pathologie

Source PubMed · Recherche par auteur (homonymes possibles, vérifier l'affiliation).

Transversal47

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Lupus1

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Revue générale1

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