Chronic
visceral pain is the predominant symptom of
functional gastrointestinal disorders and
chronic pancreatitis. Such
pain can impair the patients' quality of life, and can also serve as one of the principal reasons for these patients to seek medical help. Nevertheless, the underlying mechanisms of chronic
visceral pain have remained unclear, and much of what we know about
visceral pain has been derived from studies of somatic nociception. Current treatment of chronic
visceral pain has continued to be unsatisfactory, because of unclear pathophysiology. However, recent progress in
pain research has identified the important role of spinal microglia in the development of somatic nociception. For
visceral pain, several animal studies have demonstrated that spinal cord microglia is activated during the development of visceral
hyperalgesia, which can be induced by neonatal colorectal irritation, psychological stress, and trinitrobenzene
sulfonic acid-induced
pancreatitis. This visceral
hyperalgesia is also associated with elevated phosphorylation of
p38 mitogen-activated protein kinase.
Minocycline (a microglia inhibitor) reversed the
hyperalgesia in rat models of chronic
visceral pain, whereas
fractalkine (FKN, a microglia activator) reproduced the visceral nociception in naïve rats. These preliminary results support the pronociceptive role of spinal microglia in mediating visceral
hyperalgesia. Consequently, spinal microglia may serve as a promising target for controlling the chronic
visceral pain.