✦ LIBER ✦

Contribution of the activation of satellite glia in sensory ganglia to pathological pain

✍ Scribed by Mamoru Takeda; Masayuki Takahashi; Shigeji Matsumoto

Publisher: Elsevier Science
Year: 2009
Tongue: English
Weight: 561 KB
Volume: 33
Category: Article
ISSN: 0149-7634
DOI: 10.1016/j.neubiorev.2008.12.005

No coin nor oath required. For personal study only.

✦ Synopsis

Peripheral 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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