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Alban Latremoliere PhD

Research Fellow

Background and Research Interests
I obtained my Ph.D in neurosciences in 2007 from the University of Pierre et Marie Curie – Paris VI (UPMC; Paris, France). My Ph.D focused on facial neuropathy , a particularly debilitating form of chronic pain. The main body of my research determined the pathophysiological mechanisms underlying cephalic (facial) and extra-cephalic (rest of the body) neuropathic pain-like behaviors are different [1-3]. Our results strongly suggest that IL-6 could be one of the promoters of the signaling cascades occurring in the central nervous system that lead to abnormal pain-like behaviors after extra-cephalic, but not cephalic peripheral nerve injury [1, 4-4]. Accordingly, these data give a possible rational to why facial neuropathic pain responds poorly to treatments otherwise (relatively) effective against extra-cephalic neuropathic pain (e.g. morphine, tricyclic antidepressants, anticonvulsants) [4]. During my Ph.D, I also worked on novel approaches to study pain-like mechanisms using viral-driven gene transfer, with vectors such as herpes simplex virus [5] or lentivirus [6].

I joined Clifford Woolf’s lab in January 2008 as a postdoctoral fellow. As a pain physiologist, I am very interested by the formidable plasticity exhibited by the nociceptive system in response to either pathological (chronic inflammation, peripheral nerve injury) or non-pathological stimuli (nociceptive barrage) that occur both at the peripheral (PNS) and central nervous systems (CNS)[7, 8]. My work focuses on understanding the mechanisms that drive this plasticity at the molecular level and determine the consequences at the physiological level. To achieve this, I work to find pertinent ways to assess behavioral manifestations of nociceptive activity in rodents and characterize the associated changes in the PNS/CNS using molecular and cellular tools. When systems of interest are identified, I use genetic tools to further define their role in pain physiology.

Selected Publications

  1. Latremoliere, A.; Mauborgne, A.; Masson, J.; Bourgoin, S.; Kayser, V.; Hamon, M.; Pohl, M., Differential implication of proinflammatory cytokine interleukin-6 in the development of cephalic versus extracephalic neuropathic pain in rats. J Neurosci 2008, 28, (34), 8489-501.
  2. Kayser, V.; Viguier, F.; Ioannidi, M.; Bernard, J. F.; Latremoliere, A.; Michot, B.; Vela, J. M.; Buschmann, H.; Hamon, M.; Bourgoin, S., Differential anti-neuropathic pain effects of tetrodotoxin in sciatic nerve- versus infraorbital nerve-ligated rats--behavioral, pharmacological and immunohistochemical investigations. Neuropharmacology 2010, 58, (2), 474-87.
  3. Doucet, E.; Latremoliere, A.; Darmon, M.; Hamon, M.; Emerit, M. B., Immunolabelling of the 5-HT 3B receptor subunit in the central and peripheral nervous systems in rodents. Eur J Neurosci 2007, 26, (2), 355-66.
  4. Hamon, M.; Kayser, V.; Bourgoin, S., [Neuropathic pain. Physiopathological mechanisms and therapeutic perspectives]. Bull Acad Natl Med 2008, 192, (5), 921-6; discussion 926-8.
  5. Meunier, A.; Latremoliere, A.; Mauborgne, A.; Bourgoin, S.; Kayser, V.; Cesselin, F.; Hamon, M.; Pohl, M., Attenuation of pain-related behavior in a rat model of trigeminal neuropathic pain by viral-driven enkephalin overproduction in trigeminal ganglion neurons. Mol Ther 2005, 11, (4), 608-16.
  6. Meunier, A.; Latremoliere, A.; Dominguez, E.; Mauborgne, A.; Philippe, S.; Hamon, M.; Mallet, J.; Benoliel, J. J.; Pohl, M., Lentiviral-mediated targeted NF-kappaB blockade in dorsal spinal cord glia attenuates sciatic nerve injury-induced neuropathic pain in the rat. Mol Ther 2007, 15, (4), 687-97.
  7. Latremoliere, A.; Woolf, C. J., Central sensitization: a generator of pain hypersensitivity by central neural plasticity. J Pain 2009, 10, (9), 895-926.
  8. Costigan, M.; Moss, A.; Latremoliere, A.; Johnston, C.; Verma-Gandhu, M.; Herbert, T. A.; Barrett, L.; Brenner, G. J.; Vardeh, D.; Woolf, C. J.; Fitzgerald, M., T-cell infiltration and signaling in the adult dorsal spinal cord is a major contributor to neuropathic pain-like hypersensitivity. J Neurosci 2009, 29, (46), 14415-22.

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