Abstract
Pain is divided into two groups: physiological pain (nociceptive pain) and pathological pain. Although physiological pain is adaptive, transient, and has a protective role as a warning signal of potential tissue damage in response to a noxious stimulus, pathological clinical pain is usually maladaptive, persists, and serves no meaningful defensive or other helpful purpose. Peripheral tissue injury and inflammation are known to alter the properties of somatic sensory pathways, resulting in behavioral hypersensitivity and pathological pain, including increased responses to pain caused by both noxious stimuli (hyperalgesia) and normally innoxious stimuli (allodynia). It has been reported that glia cells in the spinal cord contribute to the maintenance of pathological pain, but recent evidence suggests that activation of satellite glia in sensory ganglia may also plays a significant 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 present review focused on the function of satellite glia cells in sensory ganglia to pathological pain. Furthermore, we discuss potential therapeutic targets in satellite glia-neuronal interactions for the prevention of pathological pain.
