Pathophysiological implication of CaV3.1 T-type Ca2+ channels in trigeminal neuropathic pain

Author:

Choi Soonwook,Yu Eunah,Hwang Eunjin,Llinás Rodolfo R.

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 Ca2+ 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.

Funder

HHS | NIH | National Institute of Neurological Disorders and Stroke

University of Science and Technology

National Research Foundation of Korea

Korea Institute of Science and Technology

Global Frontier Resarch and Development Program

Publisher

Proceedings of the National Academy of Sciences

Subject

Multidisciplinary

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