Commonalities between pain and memory mechanisms and their meaning for understanding chronic pain.
Pain sensing neurons in the periphery (called nociceptors) and the central neurons that receive their projections show remarkable plasticity following injury. This plasticity results in amplification of pain signaling that is now understood to be crucial for the recovery and survival of organisms following injury. These same plasticity mechanisms may drive a transition to a nonadaptive chronic pain state if they fail to resolve following the termination of the healing process. Remarkable advances have been achieved in the past two decades in understanding the molecular mechanisms that underlie pain plasticity following injury. The mechanisms bear a striking resemblance to molecular mechanisms involved in learning and memory processes in other brain regions, including the hippocampus and cerebral cortex. Here those mechanisms, their commonalities and subtle differences, will be highlighted and their role in causing chronic pain will be discussed. Arising from these data is the striking argument that chronic pain is a disease of the nervous system, which distinguishes this phenomena from acute pain that is frequently a symptom alerting the organism to injury. This argument has important implications for the development of disease modifying therapeutics.
Behavioral and Brain Sciences, The University of Texas at Dallas, Richardson, Texas, USA. Electronic address: theodore.price@utdallas.edu.
Theodore J
TJ
Price
Behavioral and Brain Sciences, The University of Texas at Dallas, Richardson, Texas, USA.
Kufreobong E
KE
Inyang
D000818:Animals; D059350:Chronic Pain / Q000503:physiopathology*; D006801:Humans; D008568:Memory; D008959:Models, Neurological; D009619:Nociceptors / Q000378:metabolism; D014176:Protein Biosynthesis; D066148:Spinal Cord Dorsal Horn / Q000473:pathology
AMPK; Atypical PKC; Axonal mRNA; BDNF; CREB; ERK; Hyperalgesic priming; IL-6; LTP; NGF; Opioid; PKMzeta; Reconsolidation; eIF4E; mTOR; trkB