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Neuropathic Pain Discovery, in Canada!
Click here for the NeuroScience Canada Press Release. In the Press Release you will find a quote from current Canadian Ambassador to the USA, the Honourable Michael Wilson, regarding the immense cost to society.
The Research Centres:
Division de Neurobiologie Cellulaire, Centre de Recherche Universite´ Laval Robert-Giffard, Quebec
Department of Pharmacology & Therapeutics, McGill University, Montreal, Quebec
Programme in Brain and Behaviour, The Hospital for Sick Children, 555 University Avenue, Toronto
Department of Molecular and System Pharmacology, Graduate School of Pharmaceutical Sciences, Kyushu University, Higashi, Fukuoka, Japan
Division de Neurobiologie Systemique, Centre de recherche Universite´ Laval Robert-Giffard, Quebec
Departement de Psychiatrie, Universite´ Laval, Quebec
(Reproduced with permission - Torstar Syndication Services)
Click here for the NeuroScience Canada 'Brain Repair Team' under Dr. Salter and Dr. Yves De Koninck.
Nature, December 15th.- BDNF from microglia causes the shift in neuronal anion gradient underlying neuropathic pain
On the importance of the Canadian neuropathic pain discovery:
"This is an important study because it is an important step toward
understanding how dorsal horn neurons in the spinal cord become more
sensitive to nociceptive input. This increased sensitivity is thought to be
an important part of the processes involved in the transition from acute to
chronic pain. Although this is a basic science study and doesn't directly
address the pathophysiology of FM, a better understanding of these process
may eventually lead to treatments for chronic pain conditions such as FM."
Dr. Warren Nielson
Beryl & Richard Ivey Rheumatology Day Programs
St. Joseph's Health Care London
"Thank you, .for the MOST uplifting report we've had in - well, forever. A
happy Christmas indeed,..."
Beth Ediger
Canadian FM researcher
Editor of the Quarterly FM research review, found at fm-cfs.ca
"Mike Salter and his colleagues are outstanding world-wide in the
investigation of the neural and neurochemical bases of pain..."
Dr. Harold Merskey
Professor Emeritus of Psychiatry
University of Western Ontario, London, Ontario
"...This should be very important; I have followed the research on glia with great interest over the past few years. Glial cell activation in the spinal cord (likely also brain) is the best explanation for FM that we currently have...."
Dr. Ellen Thompson, MB BS,FRCPC
Anaesthesiologist, (Anaesthesia & Chronic Pain Management), Clinical Assistant Professor, U. Ottawa
Member: Canadian Pain Society, the American Pain Society, the International Assn for the Study of Pain
"...it is making a buzz in the legal circle of lawyers who represent injured clients..."
Ted Masters
Burke Robertson
Thank you for making me aware of the recent findings by Dr. Michael Salter and colleagues in Canada. The abstract you provided indicates that they have observed that neuronal injury can cause microglia to produce a protein or peptide which alters the effects of gama-amino-butyric acid receptor [GABAr] activation. Since GABAr activation is expected to inhibit neural processing of pain signals, this alteration would facilitate pain instead. This effect might be comparable to switching the location of the gas pedal on a motor vehicle to the location of the brake pedal. The unsuspecting driver would drastically increase speed just when the perception is that slowing down would be prudent.
There have been suspicions for some time now that the microglia cells are not inert to neural functions. There is evidence that inflammation among these cells may contribute to the process of central nervous system injury in patients with Alzheimers disease (1). Similarly, there is evidence that soluble products from microglia may be facilitating pain in animals with experimental nerve injury that would mimic the human neuropathic state and cause allodynia (2-4). Interestingly, it has already been noted that minocycline can inhibit the microglia inflammation process.
The direction of this research is as relevant to central neuropathic disorders like the fibromyalgia syndrome as it is to peripheral neuropathic conditions like diabetic neuropathy or traumatic injury to the sciatic nerve. It is also important because there are active efforts to develop medications that activate the GABAr with the perception that GABAr activation would inhibit the neuropathic pain and allodynia. If the findings of Salter and colleagues are confirmed, the search for GABAr agonists to treat neuropathic pain may be heading in the wrong direction. There is more than one type of GABAr, so it will be important to learn which of these receptors types is altered by the microglia protein product.
I. Jon Russell, MD, PhD
Associate Professor of Medicine
Director, University Clinical Research Center
The University of Texas Health Science Center at San Antonio
Editor, Journal of Musculoskeletal Pain
Reference List
1. Halliday G, Robinson SR, Shepherd C, Kril J: Alzheimer's disease and inflammation: a review of cellular and therapeutic mechanisms. [Review] [75 refs]. Clinical & Experimental Pharmacology & Physiology 27: 1-8, 2000.
2. Ledeboer A, Sloane EM, Milligan ED, Frank MG, Mahony JH, Maier SF, Watkins LR: Minocycline attenuates mechanical allodynia and proinflammatory cytokine expression in rat models of pain facilitation. Pain 115: 71-83, 2005.
3. Milligan ED, Zapata V, Chacur M, Schoeniger D, Biedenkapp J, O'Connor KA, Verge GM, Chapman G, Green P, Foster AC, Naeve GS, Maier SF, Watkins LR: Evidence that exogenous and endogenous fractalkine can induce spinal nociceptive facilitation in rats. European Journal of Neuroscience 20: 2294-2302, 2004.
4. Watkins LR, Milligan ED, Maier SF: Glial proinflammatory cytokines mediate exaggerated pain states: implications for clinical pain. [Review] [162 refs]. Advances in Experimental Medicine & Biology 521: 1-21, 2003.
Additional links to research on Microglia
Understanding the Brain - The Brain from Top to Bottom
Click here - www.thebrain.mcgill.ca
February 16, 1998, Dartmouth Medical School researchers identify new mechanism underlying pain
Click here
April 6, 2005, Dartmouth Medical School researchers demonstrate a receptor in CNS immune cells plays a critical role in neuropathic pain
Click here
Human Forebrain Mechanisms of Normal and Aberrant Pain States - McGill U., slides
Click here
Signal transduction and the immune system, The Scientist magazine feature article
Click here
Neuroimmune Activation and Neuroinflammation in Chronic Pain and Opioid Tolerance/Hyperalgesia
Click here
April, 15th, 2005, Max Planck Researchers shed light on the immune defense behaviour of Microglial cells in the brain
Click here
2004, Proceedings of the 10th World Congress on Pain
Click here
Microglia images on Google
Click here
Role of Neuronal/Glial Cell Interactions in Orofacial Pain Disorders
Click here
Research to identify key factors produced in neuronal and glial cells that contribute to degenerative processes
Click here
June 24, 2003, Impaired neuropathic pain responses in mice lacking the chemokine receptor CCR2
Click here
Functional magnetic resonance imaging evidence for midbrain reticular formation involvement in a human model of neuropathic pain
Click here
2003, Researchers now highlight an important role for G-protein-coupled chemokine receptors in the processing of chronic pain signals
Click here
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