Le resvératrol issu du vin et ses effets sur la santé

BORDEAUX2-BU Santé (330632101) / SudocSudocFranceF

Immunohistochemical localization of the carboxy terminus of the novel mu opioid receptor splice variant MOR-IC within the human spinal cord

The present study examined the distribution in the human spinal cord of a unique carboxy terminus sequence contained within MOR-IC, one of the recently described splice variants of the cloned mu opioid receptor gene MOR-I. Although MOR-I-like immunoreactivity (LI) and delta opioid receptor-like immunoreactivity were observed only in the superficial laminae, MOR-IC-LI was abundant in the superficial laminae of the dorsal horn and around the central canal. In the substantia gelatinosa, MOR-IC-LI was found in small diameter axonal elements, the cytoplasm and the plasmalemma of small spinal neurons and dendrites in inner lamina II and in some fibers within Lissauerʼs tract. These studies imply the presence of MOR-IC in human spinal cord and its distribution suggests that it plays a role in the control of pain processing

Bilan et enjeux du programme interdisciplinaire Ingeco du CNRS (2007-2011): un tournant pour l’ingénierie écologique en France

International audienceNous présentons un bilan du Programme interdisciplinaire de recherche (PIR) « Ingénierie écologique » (Ingeco, CNRS/Irstea). Nous montrons la contribution de ce programme à l’émergence et à la structuration d’une réelle communauté française de recherche sur l’ingénierie écologique

Bilan et enjeux du programme interdisciplinaire Ingeco du CNRS (2007-2011): un tournant pour l’ingénierie écologique en France

International audienceNous présentons un bilan du Programme interdisciplinaire de recherche (PIR) « Ingénierie écologique » (Ingeco, CNRS/Irstea). Nous montrons la contribution de ce programme à l’émergence et à la structuration d’une réelle communauté française de recherche sur l’ingénierie écologique

Chemokines and pain mechanisms

The development of new therapeutic approaches to the treatment of painful neuropathies requires a better understanding of the mechanisms that underlie the development of these chronic pain syndromes. It is now well established that astrocytic and microglial cells modulate the neuronal mechanisms of chronic pain in spinal cord and possibly in the brain. In animal models of neuropathic pain following peripheral nerve injury, several changes occur at the level of the first pain synapse between the central terminals of sensory neurons and second order neurons. These neuronal mechanisms can be modulated by pronociceptive mediators released by non neuronal cells such as microglia and astrocytes which become activated in the spinal cord following PNS injury. However, the signals that mediate the spread of nociceptive signaling from neurons to glial cells in the dorsal horn remain to be established. Herein we provide evidence for two emerging signaling pathways between injured sensory neurons and spinal microglia: chemotactic cytokine ligand 2 (CCL2)/CCR2 and cathepsin S/CX3CL1 (fractalkine)/CX3CR1. We discuss the plasticity of these two chemokine systems at the level of the dorsal root ganglia and spinal cord demonstrating that modulation of chemokines using selective antagonists decrease nociceptive behavior in rodent chronic pain models. Since up-regulation of chemokines and their receptors may be a mechanism that directly and/or indirectly contributes to the development and maintenance of chronic pain, these molecular molecules may represent novel targets for therapeutic intervention in sustained pain states