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Pathological Pain: From Molecular to Clinical Aspects by Novartis Foundation

By Novartis Foundation

This publication brings jointly contributions from key investigators within the region of pathological pain.  It covers the molecular foundation of receptors and channels focused on nociception, the prospective messages that reason neuropathic plasticity, spinal plasticity in neuropathy, plastic adjustments in opioid platforms in neuropathy and opioid tolerance, and plastic alterations with regards to pathological pain.


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Extra resources for Pathological Pain: From Molecular to Clinical Aspects

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3, working against a voltage-insensitive passive K+ leak conductance, probably one of the 2P channels (Amir et al 2002). In contrast, when you block the voltage-sensitive K+ channels in the cell this strongly facilitates the oscillations, and enhances repetitive ¢ring. Norepinephrine will do this, for example. We had always thought that norepinephrine activates injured sensory neurons by depolarization. Instead, its primary mode of action in causing ectopic ¢ring may turn out to be that it makes the neurons more resonant.

3 mRNA and protein go up in the DRG of the injured segment. 8 goes up in the uninjured segment. 8 seem to go in opposite directions. Wood: I was fascinated by your observation that the ectopic discharges arose from the somata, yet the neuroma presumably makes a contribution. What is the role of the neuroma? Chung: We have looked at where the ectopic discharge originates. When we ligate the spinal nerve very close to the DRG, most of the activity comes from the DRG. But when we make a further injury distally, the situation seems to change.

9 might be useful for the treatment of pain. 9 persistent current and its depolarizing in£uence on resting potential (Cummins et al 1999) might remove resting inactivation from other sodium channels. 9 null mutants or selective blockers, there is inadequate information on the role of this channel in neuropathic pain, although normal level of expression seems to be dependent on the supply of NGF or glial cell-derived neurotrophic factor (GDNF) (Cummins et al 2000). 9 current densities can be upregulated in the presence of GTP or its non-hydrolysable analogue GTPgS.

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