Experimental neurology
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Experimental neurology · Feb 2013
Comparative StudyDifferential effects of activity dependent treatments on axonal regeneration and neuropathic pain after peripheral nerve injury.
Activity treatments are useful strategies to increase axonal regeneration and functional recovery after nerve lesions. They are thought to benefit neuropathy by enhancing neurotrophic factor expression. Nevertheless the effects on sensory function are still unclear. ⋯ ES speeded up expression of BDNF and GDNF in DRG, and of BDNF and NT3 in the ventral horn. TR reduced the levels of pro-nociceptive factors such as BDNF, NGF and GDNF in DRG. Combination of ES and TR induced intermediate levels suggesting an optimal balancing of treatment effects.
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Experimental neurology · Feb 2013
Selectively reducing cytokine/chemokine expressing macrophages in injured nerves impairs the development of neuropathic pain.
It has been well documented that Wallerian degeneration following nerve injury is associated with inflammatory reaction. Such local inflammation contributes to the development of chronic neuropathic pain. Macrophages are one of the major players in the process of either or both degeneration/regeneration and hypersensitivity. ⋯ Very interestingly, local TGF-β1 treatment had no effect on the population of ED1(+) phagocytic macrophages. In addition to its effect on selective subsets of macrophages, TGF-β1 also reduced T-lymphocyte infiltration. Our results revealed the critical roles of cytokine/chemokine secreting MAC1(+) macrophages in the development of neuropathic pain, and highlighted the needs and benefits of targeting specific populations of macrophages in alleviating neuropathic pain without delaying nerve regeneration.
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Experimental neurology · Feb 2013
Hydrogen sulfide inhibits preoptic prostaglandin E2 production during endotoxemia.
Hydrogen sulfide (H(2)S) is a gaseous neuromodulator endogenously produced in the brain by the enzyme cystathionine β-synthase (CBS). We tested the hypothesis that H(2)S acts within the anteroventral preoptic region of the hypothalamus (AVPO) modulating the production of prostaglandin (PG) E(2) (the proximal mediator of fever) and cyclic AMP (cAMP). To this end, we recorded deep body temperature (Tb) of rats before and after pharmacological modulation of the CBS-H(2)S system combined or not with lipopolysaccharide (LPS) exposure, and measured the levels of H(2)S, cAMP, and PGE(2) in the AVPO during systemic inflammation. ⋯ The LPS-induced decreased levels of cAMP were reduced to a lesser extent by the H(2)S donor. The LPS-induced PGE(2) production was potentiated by AOA (the CBS inhibitor) and inhibited by the H(2)S donor. Our data are consistent with the notion that the gaseous messenger H(2)S synthesis is downregulated during endotoxemia favoring PGE(2) synthesis and lowering cAMP levels in the preoptic hypothalamus.