RRC ID 40055
著者 Choi S, Yu E, Hwang E, Llinás RR.
タイトル Pathophysiological implication of CaV3.1 T-type Ca2+ channels in trigeminal neuropathic pain.
ジャーナル Proc Natl Acad Sci U S A
Abstract 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 CaV3.1 T-type Ca(2+) channel knockout and wild-type mice. CaV3.1 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 in wild-type mice but not in CaV3.1 knockout mice. Our results suggest that the presence of CaV3.1 channels is a key element in the pathophysiology of trigeminal neuropathic pain.
巻・号 113(8)
ページ 2270-5
公開日 2016-2-23
DOI 10.1073/pnas.1600418113
PII 1600418113
PMID 26858455
PMC PMC4776481
MeSH Animals Calcium Channels, T-Type / deficiency Calcium Channels, T-Type / genetics Calcium Channels, T-Type / physiology* Delta Rhythm / genetics Delta Rhythm / physiology Electrophysiological Phenomena Female Gamma Rhythm / genetics Gamma Rhythm / physiology Male Mice Mice, Inbred C57BL Mice, Knockout Neuralgia / genetics Neuralgia / physiopathology* Somatosensory Cortex / physiopathology Thalamic Nuclei / physiopathology Trigeminal Neuralgia / genetics Trigeminal Neuralgia / physiopathology*
IF 9.412
引用数 19
WOS 分野 NEUROSCIENCES
リソース情報
実験動物マウス RBRC01465