Hi,
I was just wondering if the mechanism of action potential generation constrains the brain into only reacting to external stimuli and never on its own.
I'm lost with this statement since brain is made by neurons and of course they are neurons that are kind of clock/timers that fire continuously and the rate are modified by some other neurons.
Are you talking about potentiation/depression (LTP /LTD)? And I thought allodynia was increased pain sensitivity due to subthreshold injury to the peripheral pain receptors!
No I'm talking about neurons that are changing of behaviour:
J Neurophysiol 90: 1949-1955, 2003. First published April 30, 2003; 10.1152/jn.00175.2003
0022-3077/03
Inflammation Induces Ectopic Mechanical Sensitivity in Axons of Nociceptors Innervating Deep Tissues
Geoffrey M. Bove1, Bernard J. Ransil2, Hsi-Chiang Lin1 and Jeong-Gill Leem1
1 Department of Anesthesia and Critical Care Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215; 2 Department of Neurology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215
Submitted 25 February 2003; accepted in final form 30 April 2003
A variety of seemingly diverse pain syndromes are characterized by movement-induced pain radiating in the distribution of a peripheral nerve or nerve root. This could be explained by the induction of ectopic mechanical sensitivity in intact sensory axons. Here we show that inflammation led to mechanical sensitivity of the axons of a subset of mechanically sensitive primary sensory neurons. Dorsal root recordings were made from 194 mechanically sensitive neurons that innervated deep and cutaneous structures and had C, A alpha, and A delta conduction velocities. No axons of any category were mechanically sensitive in control experiments. However, the axons of neurons innervating deep structures and having C- or A delta -conduction velocities became mechanically sensitive during the neuritis, and also exhibited an increased incidence of spontaneous discharge. The incidence of mechanical sensitivity followed a distinct time course. In some cases, paw withdrawal thresholds were obtained after neuritis induction. The time course of the resultant hypersensitivity was not directly related to the time course of the axonal mechanical sensitivity. Ectopic axonal mechanical sensitivity could explain some types of radiating, nerve-related pain coexisting with diseases of seemingly diverse etiologies.
Address for reprint requests: G. M. Bove, Department of Anesthesia and Critical Care, Beth Israel Deaconess Medical Center, 330 Brookline Ave., Dana 721, Boston, MA 02215 (E-mail:
gbove@bidmc.harvard.edu).