|
|
||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Institute of Physiology and Pathophysiology, Johannes Gutenberg-University, Mainz, Germany
* To whom correspondence should be addressed. E-mail: treede{at}uni-mainz.de.
As in neocortex and hippocampus, neurons in the dorsal horn of the spinal cord develop long-term potentiation of synaptic efficacy (LTP) upon high-frequency stimulation (HFS) of their afferent input, but how long LTP lasts in this nociceptive relay nucleus has not yet been addressed. We now studied neurogenic hyperalgesia, a perceptual correlate of nociceptive LTP, in 13 healthy subjects, following HFS (5 x 1s at 100Hz) of superficial cutaneous afferents. HFS led to a mean upward shift of the stimulus-response function for pinprick-evoked pain (punctate mechanical hyperalgesia) in all subjects by a factor of 2.5 (p<0.001) that lasted undiminished for the initial one-hour observation period. Follow-up tests until the next day revealed that this type of neurogenic hyperalgesia decayed with a t1/2 of 3.3h (99% CI: 3.1-3.5h), and disappeared completely within 25.4h (99% CI: 20.4-31.6h). Touch-evoked pain (dynamic mechanical allodynia) developed in 8/13 subjects, decayed with a t1/2 of 2.9h from the maximum and disappeared within 9.3h. These findings suggest that a single HFS session induces nociceptive LTP in healthy subjects that corresponds to early-LTP (LTP1), implying primarily posttranslational mechanisms for this type of plasticity of human pain perception.
This article has been cited by other articles:
![]() |
S. M. Geranton, C. Morenilla-Palao, and S. P. Hunt A Role for Transcriptional Repressor Methyl-CpG-Binding Protein 2 and Plasticity-Related Gene Serum- and Glucocorticoid-Inducible Kinase 1 in the Induction of Inflammatory Pain States J. Neurosci., June 6, 2007; 27(23): 6163 - 6173. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |