Targeting central plasticity: a new direction of finding painkillers.
It is well documented that sensory transmission, including pain, receives endogenous inhibitory modulatory influences at dorsal horn of the spinal cord. Recent results, from behavioral to molecular studies, demonstrate that injury caused plastic changes in forebrain areas. In addition to encoding pain, these supraspinal areas may also affect pain transmission in the spinal cord level by activating "top-down" descending facilitatory systems. In this review, I provide review of evidence related to these new progresses, from human brain imaging to work from genetically mutant mice.
Zhuo
Min
M
Department of Physiology, Faculty of Medicine, University of Toronto Center for the Study of Pain, University of Toronto, Toronto, Ontario M5S 1A8, Canada. min.zhuo@utoronto.ca
D000700:Analgesics / Q000494:pharmacology*; D000818:Animals; D002118:Calcium / Q000494:pharmacology; D002490:Central Nervous System / Q000187:drug effects*; D002540:Cerebral Cortex / Q000503:physiopathology; D002908:Chronic Disease; D005786:Gene Expression Regulation / Q000187:drug effects / Q000502:physiology; D006801:Humans; D009473:Neuronal Plasticity / Q000187:drug effects* / Q000235:genetics; D010146:Pain / Q000188:drug therapy* / Q000235:genetics / Q000503:physiopathology; D016194:Receptors, N-Methyl-D-Aspartate / Q000187:drug effects; D017981:Receptors, Neurotransmitter / Q000187:drug effects; D013569:Synapses / Q000187:drug effects / Q000235:genetics / Q000502:physiology; D009435:Synaptic Transmission / Q000187:drug effects / Q000235:genetics / Q000502:physiology
D000700:Analgesics; D016194:Receptors, N-Methyl-D-Aspartate; D017981:Receptors, Neurotransmitter; D002118:Calcium