By Martin Michaelis (auth.), Annika B. Malmberg PhD, Sandra R. Chaplan MD (eds.)
Numerous advancements in our knowing of the mechanisms that underlie neuropathic soreness states have come from the improvement of animal versions, so much of which contain partial peripheral nerve damage. The animal versions have proven that nerve harm initiates a cascade of occasions leading to altered neurochemistry and molecular biology of the peripheral neurons, the dorsal root ganglion mobile, and adjustments in neurotransmitter and receptor expression within the dorsal horn of the spinal wire. furthermore, nerve damage produces anatomical alterations with practical outcomes.
This quantity summarises the present knowing of the pathophysiological approaches within the peripheral and vital frightened procedure that give a contribution to the neuropathic ache. It offers a well timed assessment of neuropathic ache mechanisms, written by means of specialists within the field.
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Additional resources for Mechanisms and Mediators of Neuropathic Pain
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I. Sodium currents. Neuroscience 6: 2423-2430 Roy ML, Narahashi T (1992) Differential properties of tetrodotoxin-sensitive and tetrodotoxin-resistant sodium channels in rat dorsal root ganglion neurons. ] Neurosci 12: 2104-2111 Caffrey ]M, Eng DL, Black ]A, Waxman SG, Kocsis ]D (1992) Three types of sodium channels in adult rat dorsal root ganglion neurons. Brain Res 592: 283-297 Elliott AA, Elliott]R (1993) Characterization of TTX-sensitive and TTX-resistant sodium currents in small cells from adult rat dorsal root ganglia.
1I11. (C) Recovery from inactivation is accelerated after CCI. Repriming kinetics of CO neurons are intermediate between values obtained for control and peripherally-axotomized neurons. Modified and reproduced with permission from [64J. els are significantly lower in small CO neurons compared to control neurons. (E) Representative TTX-resistant sodium currents in control and CO small neurons. (F) Mean TTX-resistant peak current densities from control and CO neurons. The TTX-resistant current density is significantly smaller in CO neurons.