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Canadian Association of Neuroscience Review: Cellular and Synaptic Insights into Physiological and Pathological Pain

Published online by Cambridge University Press:  02 December 2014

Min Zhuo*
Affiliation:
Department of Physiology, Faculty of Medicine, University of Toronto, Centre for the Study of Pain, University of Toronto, Toronto, ON, Canada
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Abstract

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Neurons and synapses in the central nervous system are plastic, undergoing long-term changes throughout life. Studies of molecular and cellular mechanisms of such changes not only provide important insight into how we learn and store new knowledge in our brains, but they also reveal the mechanisms of pathological changes that occur following injury. The author proposes that during induction, neuronal mechanisms underlying physiological functions, such as learning and memory, may share some common signaling molecules with abnormal or injury-related changes in the brain. Distinct synaptic and neuronal network mechanisms are involved in pathological pain as compared to cognitive learning and memory. Nociceptive information is transmitted and regulated at different levels of the brain, from the spinal cord to the forebrain. Furthermore, N-methyl-D-aspartate receptor-dependent and calcium-calmodulin activated adenylyl cyclases (AC1 and AC8) in the anterior cingulate cortex play important roles in the induction and expression of persistent inflammatory and neuropathic pain. Neuronal activity in the anterior cingulate cortex can also influence nociceptive transmission in the dorsal horn of the spinal cord by activating the endogenous facilitatory system. Our results provide important synaptic and molecular insights into physiological responses to injury.

Résumé:

RÉSUMÉ:

Les neurones et les synapses du système nerveux central sont plastiques et subissent des changements à long terme pendant toute la vie. Des Études sur les mÉcanismes molÉculaires et cellulaires impliquÉs dans ces changements fournissent des informations importantes sur les mÉcanismes d’apprentissage et de storage de nouvelles connaissances ainsi que sur les mÉcanismes impliquÉs dans les changements pathologiques suite à une lÉsion. L’auteur propose que pendant l’induction, des molÉcules qui servent à la signalisation et qui sont impliquÉes dans les mÉcanismes neuronaux sous-jacents aux fonctions physiologiques comme l’apprentissage et la mÉmoire, sont Également impliquÉes dans les changements observÉs suite à une lÉsion cÉrÉbrale. Les mÉcanismes au niveau des rÉseaux synaptiques et neuronaux sont diffÉrents dans la douleur pathologique et dans l’apprentissage cognitif et la mÉmoire. L’information nociceptive est transmise et rÉgulÉe à diffÉrents niveaux du cerveau, de la moelle Épinière au prosencÉphale. De plus, l’adÉnyl-cyclase dÉpendante du rÉcepteur N-mÉthyl-D-aspartate et l’adÉnyl-cyclase activÉe par le couple calcium/calmodulin (AC1 et AC8) dans le cortex cingulaire antÉrieur jouent des rôles importants dans l’induction et l’expression de la douleur persistante d’Étiologie inflammatoire et nÉvropathique. L’activitÉ neuronale dans le cortex cingulaire antÉrieur peut aussi influencer la transmission nociceptive dans la corne postÉrieure de la moelle Épinière en activant le système facilitateur endogène. Nos rÉsultats contribuent à la comprÉhension des mÉcanismes synaptiques et molÉculaires impliquÉs dans la rÉponse physiologique à une lÉsion.

Type
Review Article
Copyright
Copyright © The Canadian Journal of Neurological 2014

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