UTCSP External Review Reports Now Available On-line
The University of Toronto Centre for the Study of Pain underwent an External Review in early October, 2008. The review team consisted of Dr. Troels Jensen, Director of the Danish Pain Research Centre at Aarhus University Hospital, Denmark, immediate past-President of the International Association for the Study of Pain, and Dr. Mary Ellen Jeans, President & CEO of Associated Medical Services, former CEO of the Canadian Nurses Association and former Director of the School of Nursing at McGill University. A PDF of the UTCSP External Review Report, along with the reviewer’s report is now available: UTCSP External Review Report 2008; Reviewer's Report of the UTCSP
Salter team reports discovery of a novel approach to treating chronic pain by blocking an intracellular protein interaction in the central nervous system
Mike Salter’s research team has developed a peptide for treating pain by blocking an intracellular protein interaction in the central nervous system (CNS). The team’s findings are reported in the December issue of Nature Medicine. The conventional understanding is that chronic pain hypersensitivity is dependent upon N-methyl-D-aspartate receptors (NMDARs), a main subtype of glutamate receptor mediating communication between neurons in the CNS. However, treating chronic pain through the use of NMDAR blocking drugs is limited because NMDARs are essential for many key physiological functions. Salter’s team discovered that pain hypersensitivity depends upon amplification of the function of NMDARs by the protein tyrosine kinase Src. Using rodent models, the team designed a peptide that, when given intravenously, is able to prevent the action of Src to amplify NMDAR function. This was achieved by designing the peptide to disrupt the interaction between two proteins, Src and NADH dehydrogenase subunit 2 (ND2), which anchors Src to NMDAR. Salter’s team shows that the peptide selectively inhibits the amplification of NMDAR that produces chronic pain, without affecting physiological functions of the receptor. As the peptide suppressed pain behaviours in models of both inflammatory and neuropathic pain but did not affect acute, nociceptive pain behaviours, this approach is potentially of broad use for chronic pain disorders.