• Mamoru Takeda, Masayuki Takahashi, and Shigeji Matsumoto.
• Department of Physiology, School of Life Dentistry at Tokyo, Nippon Dental University, Chiyoda-ku, Tokyo, Japan. m-takeda@tokyo.ndu.ac.jp
• Neurosci Biobehav Rev. 2009 Jun 1;33(6):784-92.

AbstractPeripheral tissue injury/inflammation can alter the properties of somatic sensory pathways, resulting in behavioral hypersensitivity and pathological and/or chronic pain, including increased responses to pain caused by both noxious stimuli (hyperalgesia) and normally innocuous stimuli (allodynia). Although there are increasing reports that glia in the spinal cord contribute to the maintenance of pathological pain, recent evidence suggests that activation of satellite glia in sensory ganglia may also play an important role in the development of hyperalgesia and allodynia. There is evidence that non-synaptically released chemical mediators derived from both neurons and satellite glia may trigger chronic pain via autocrine and/or paracrine mechanisms and that augmented excitability of primary afferent neurons results in changes in central pain-signaling neurons (central sensitization). The focus of the present review is on the contribution of the activation of satellite glia in sensory ganglia to pathological pain. In addition, we discuss potential therapeutic targets in satellite glia-neuronal interactions for the prevention of pathological pain.

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