[Can chronic pain and spreading of pain be induced via glial mechanisms? New hypotheses on the generators maintaining protracted pain conditions].
There are various types of pain: acute, inflammatory, and neuropathic. The latter starts with a nerve injury, which could be secondary to an inflammatory reaction. Neuropathic pain often remains even after the original injury has healed and sometimes becomes chronic. It has recently been proposed that activated astrocytes and microglial cells could be the generators maintaining neuropathic pain. As astrocytes exhibit gap junction coupled networks, glia may be involved in spreading of pain sensations in form of Ca2+ oscillations or waves. Astrocytic Ca2+ oscillations induce ATP release which in turn stimulates both microglial cells and those monocytes that have crossed the blood-brain barrier, and also stimulates distant astrocyte networks and microglial cells. These activated cells release pro-inflammatory cytokines. One theory is that the Ca2+ oscillations by their induction and release of growth factors, give rise to new synapses, thereby establishing new neuronal contacts for maintaining and spreading pain sensation.
Hansson
Elisabeth
E
Institutionen för klinisk neurovetenskap, Sahlgrenska akademin vid Göteborgs universitet, Sweden. elisabeth.hansson@neuro.gu.se
Zügner
Roland
R
D001253:Astrocytes / Q000502:physiology; D002118:Calcium / Q000378:metabolism; D002908:Chronic Disease; D016207:Cytokines / Q000378:metabolism; D017629:Gap Junctions / Q000502:physiology; D006801:Humans; D009457:Neuroglia / Q000502:physiology*; D009619:Nociceptors / Q000502:physiology; D010146:Pain / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology; D011978:Receptors, Nicotinic / Q000502:physiology; D011957:Receptors, Opioid / Q000502:physiology; D009435:Synaptic Transmission / Q000502:physiology
D016207:Cytokines; D011978:Receptors, Nicotinic; D011957:Receptors, Opioid; D002118:Calcium