期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 113, 期 8, 页码 2270-2275出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1600418113
关键词
central pain; cross-frequency coupling; lateral inhibition; thalamocortical dysrhythmia
资金
- National Institutes of Health [NS13742/NS/NINDS/NIH HHS]
- University of Science and Technology in the Republic of Korea (UST Post-Doctoral Research Program)
- National Research Foundation of Korea - Korean Government [NRF-2009-352-C00111]
- Korea Institute of Science and Technology [2E25472]
- Global Frontier RD Program [NRF-M1AXA003-2011-0031525]
A crucial pathophysiological issue concerning central neuropathic pain is the modification of sensory processing by abnormally increased low-frequency brain rhythms. Here we explore the molecular mechanisms responsible for such abnormal rhythmicity and its relation to neuropathic pain syndrome. Toward this aim, we investigated the behavioral and electrophysiological consequences of trigeminal neuropathic pain following infraorbital nerve ligations in Ca(v)3.1 T-type Ca2+ channel knockout and wild-type mice. Ca(v)3.1 knockout mice had decreased mechanical hypersensitivity and reduced low-frequency rhythms in the primary somatosensory cortex and related thalamic nuclei than wild-type mice. Lateral inhibition of gamma rhythm in primary somatosensory cortex layer 4, reflecting intact sensory contrast, was present in knockout mice but severely impaired in wild-type mice. Moreover, cross-frequency coupling between low-frequency and gamma rhythms, which may serve in sensory processing, was pronounced inwild-typemice but not in Ca(v)3.1 knockout mice. Our results suggest that the presence of Ca(v)3.1 channels is a key element in the pathophysiology of trigeminal neuropathic pain.
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