Pain and learning in a spinal system: contradictory outcomes from common origins.
The long-standing belief that the spinal cord serves merely as a conduit for information traveling to and from the brain is changing. Over the past decade, research has shown that the spinal cord is sensitive to response-outcome contingencies, demonstrating that spinal circuits have the capacity to modify behavior in response to differential environmental cues. If spinally transected rats are administered shock contingent on leg extension (controllable shock), they will maintain a flexion response that minimizes shock exposure. If, however, this contingency is broken, and shock is administered irrespective of limb position (uncontrollable shock), subjects cannot acquire the same flexion response. Interestingly, each of these treatments has a lasting effect on behavior; controllable shock enables future learning, while uncontrollable shock produces a long-lasting learning deficit. Here we suggest that the mechanisms underlying learning and the deficit may have evolved from machinery responsible for the spinal processing of noxious information. Experiments have shown that learning and the deficit require receptors and signaling cascades shown to be involved in central sensitization, including activation of NMDA and neurokinin receptors, as well as CaMKII. Further supporting this link between pain and learning, research has also shown that uncontrollable stimulation results in allodynia. Moreover, systemic inflammation and neonatal hindpaw injury each facilitate pain responding and undermine the ability of the spinal cord to support learning. These results suggest that the plasticity associated with learning and pain must be placed in a balance in order for adaptive outcomes to be observed.
Baumbauer
Kyle M
KM
Department of Psychology, Texas A&M University, MS 4235, College Station, TX 77843, USA. baumbauer@tamu.edu
Young
Erin E
EE
Joynes
Robin L
RL
D000818:Animals; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2 / Q000378:metabolism; D003216:Conditioning, Operant; D007249:Inflammation / Q000503:physiopathology; D015288:Neurokinin A / Q000378:metabolism; D009473:Neuronal Plasticity / Q000502:physiology; D010146:Pain / Q000503:physiopathology*; D014176:Protein Biosynthesis; D015398:Signal Transduction; D013116:Spinal Cord / Q000503:physiopathology*
D015288:Neurokinin A; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2