Neural Plasticity Research Group

Alban Latrémolière, Ph.D.
Research Fellow

Neural Plasticity Research Group
Harvard Medical School
149 13th Street, Rm. 4309
Charlestown, Massachusetts 02129-2000
E-mail:
TEL:
FAX: 617-724-3632

Research Summary

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 work focused on facial neuropathic pain, a particularly debilitating form of chronic pain. The main body of my research has consisted of determining that the pathophysiological mechanisms underlying cephalic (facial) and extra-cephalic (rest of the body) neuropathic pain-like behaviors are different 1,2. 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 1,3. Accordingly, these data give a potential 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 the NPRG in January 2008 as a postdoctoral fellow. My current research interests focus on (A) the role of immune cells present in the central nervous system (microglia, macrophages, …) in the development and/or maintenance of chronic pain, with a special interest on the complement cascade - a major trigger of microglial ‘activation’ 7, (B) the determination of the phenotype of the dorsal root ganglion neurons that upregulate GTP Cyclohydrolase I (GCH1) after peripheral nerve injury 8 and the behavioral consequences of the deletion or over-expression of GCH1, by using transgenic mice, and (C) determining the advantages of using adeno-associated virus (AAV) as novel vectors to study and/or modulate pain-like behaviors.

Selected Articles

Latremoliere A, Mauborgne A, Masson J, Bourgoin S, Kayser V, Hamon M, Pohl M (2008) Differential implication of proinflammatory cytokine interleukin-6 in the development of cephalic versus extracephalic neuropathic pain in rats. J Neurosci 28:8489-8501.
Doucet E, Latremoliere A, Darmon M, Hamon M, Emerit MB (2007) Immunolabelling of the 5-HT 3B receptor subunit in the central and peripheral nervous systems in rodents. Eur J Neurosci 26:355-366.
Faculty of 1000 Medicine, January 6th 2009, http://www.f1000medicine.com/article/id/1138048/evaluation
Hamon M, Kayser V, Bourgoin S (2008) [Neuropathic pain. Physiopathological mechanisms and therapeutic perspectives]. Bull Acad Natl Med 192:921-926; discussion 926-928.
Meunier A, Latremoliere A, Mauborgne A, Bourgoin S, Kayser V, Cesselin F, Hamon M, Pohl M (2005) Attenuation of pain-related behavior in a rat model of trigeminal neuropathic pain by viral-driven enkephalin overproduction in trigeminal ganglion neurons. Mol Ther 11:608-616.
Meunier A, Latremoliere A, Dominguez E, Mauborgne A, Philippe S, Hamon M, Mallet J, Benoliel JJ, Pohl M (2007) Lentiviral-mediated targeted NF-kappaB blockade in dorsal spinal cord glia attenuates sciatic nerve injury-induced neuropathic pain in the rat. Mol Ther 15:687-697.
Griffin RS, Costigan M, Brenner GJ, Ma CH, Scholz J, Moss A, Allchorne AJ, Stahl GL, Woolf CJ (2007) Complement induction in spinal cord microglia results in anaphylatoxin C5a-mediated pain hypersensitivity. J Neurosci 27:8699-8708.
Tegeder I, Costigan M, Griffin RS, Abele A, Belfer I, Schmidt H, Ehnert C, Nejim J, Marian C, Scholz J, Wu T, Allchorne A, Diatchenko L, Binshtok AM, Goldman D, Adolph J, Sama S, Atlas SJ, Carlezon WA, Parsegian A, Lotsch J, Fillingim RB, Maixner W, Geisslinger G, Max MB, Woolf CJ (2006) GTP cyclohydrolase and tetrahydrobiopterin regulate pain sensitivity and persistence. Nat Med 12:1269-1277.

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