Feb 22, 2005

The dissipation of neuropathic pain paradoxically involves the presence of tumor necrosis factor-alpha (TNF)

Neuropharmacology
Tracey A IgnatowskiRobert N Spengler

Abstract

Neuropathic pain, a chronic disabling pain arising from nerve injury, develops a central component. In brain neurons, tumor necrosis factor-alpha (TNF) levels intensify and TNF-inhibition of norepinephrine (NE) release, dependent upon alpha(2)-adrenergic activation, amplifies during neuropathic pain onset. TNF-inhibition of NE release transforms to facilitation in the hippocampus of rats administered antidepressants (treat neuropathic pain), contemporaneous with decreased neuron TNF. Therefore, adrenergic drugs inhibit increased pain sensitivity (hyperalgesia) by decreasing TNF production, thereby inducing increased NE release. This study examined TNF- and alpha(2)-adrenergic-regulated NE release from hippocampal slices during both the onset and dissipation of hyperalgesia during sciatic nerve chronic constriction injury (CCI). The enhanced inhibition of NE release by TNF at peak hyperalgesia (day-8) transformed to facilitation of NE release at days 12, 14, 16, and 21 post-CCI, corresponding to dissipation of hyperalgesia. Chronic antidepressant drug administration alone to rats results in similar findings. Rats administered the antidepressant amitriptyline (10 mg/kg, i.p., 60 min) at day-8 post-CCI, no longer exhibited hyperal...Continue Reading

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Mentioned in this Paper

Plexiglas
Exertion
Salicylhydroxamic acid
Amines
Tumor Necrosis Factor-alpha
Structure of Sciatic Nerve
Neurotransmitter Uptake
Visual Analog Pain Scale
Neurotransmitter Secretion
Sciatic Neuritis

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