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The Journal of Neuroscience, July 16, 2008, 28(29):7445-7453; doi:10.1523/JNEUROSCI.1812-08.2008
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Medline Plus Health Information Neurobiology of Disease
Presynaptic and Postsynaptic Amplifications of Neuropathic Pain in the Anterior Cingulate Cortex
Hui Xu, * Long-Jun Wu, * Hansen Wang, * Xuehan Zhang, Kunjumon I. Vadakkan, Susan S. Kim, Hendrik W. Steenland, andMin Zhuo Department of Physiology, Faculty of Medicine, University of Toronto Centre for the Study of Pain, Toronto, Ontario, Canada M5S1A8
Correspondence should be addressed to Dr. Min Zhuo, Department of Physiology, University of Toronto, Faculty of Medicine, Room 3342, Medical Sciences Building, 1 King's College Circle, Toronto, Ontario, Canada M5S1A8. Email: min.zhuo{at}utoronto.ca
Neuropathic pain is caused by a primary lesion or dysfunction in the nervous system. Investigations have mainly focused on the spinal mechanisms of neuropathic pain, and less is known about cortical changes in neuropathic pain. Here, we report that peripheral nerve injury triggered long-term changes in excitatory synaptic transmission in layer II/III neurons within the anterior cingulate cortex (ACC). Both the presynaptic release probability of glutamate and postsynaptic glutamate AMPA receptor-mediated responses were enhanced after injury using the mouse peripheral nerve injury model. Western blot showed upregulated phosphorylation of GluR1 in the ACC after nerve injury. Finally, we found that both presynaptic and postsynaptic changes after nerve injury were absent in genetic mice lacking calcium-stimulated adenylyl cyclase 1 (AC1). Our studies therefore provide direct integrative evidence for both long-term presynaptic and postsynaptic changes in cortical synapses after nerve injury, and that AC1 is critical for such long-term changes. AC1 thus may serve as a potential therapeutic target for treating neuropathic pain.
Key words: anterior cingulate cortex; presynaptic release; adenylyl cyclase; AMPA receptor; mice; neuropathic pain
Received Feb. 21, 2008; revised June 6, 2008; accepted June 9, 2008.
Correspondence should be addressed to Dr. Min Zhuo, Department of Physiology, University of Toronto, Faculty of Medicine, Room 3342, Medical Sciences Building, 1 King's College Circle, Toronto, Ontario, Canada M5S1A8. Email: min.zhuo{at}utoronto.ca
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