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pubmed-article:7506046pubmed:abstractTextLeukemia inhibitory factor (LIF; also known as cholinergic differentiation factor) is a multifunctional cytokine that affects neurons, as well as many other cell types. To examine its neuronal functions in vivo, we have used LIF-deficient mice. In culture, LIF alters the transmitter phenotype of sympathetic neurons, inducing cholinergic function, reducing noradrenergic function, and altering neuropeptide expression. In vivo, a noradrenergic to cholinergic switch occurs in the developing sweat gland innervation, and changes in neuropeptide phenotype occur in axotomized adult ganglia. We find that the gland innervation of LIF-deficient mice is indistinguishable from normal. In contrast, neuropeptide induction in ganglia cultured as explants or axotomized in situ is significantly suppressed in LIF-deficient mice. Thus, LIF plays a role in transmitter changes induced by axotomy but not by developmental interactions with sweat glands.lld:pubmed
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pubmed-article:7506046pubmed:articleTitleLeukemia inhibitory factor mediates an injury response but not a target-directed developmental transmitter switch in sympathetic neurons.lld:pubmed
pubmed-article:7506046pubmed:affiliationDepartment of Neurosciences, Case Western Reserve University, Cleveland, Ohio 44106.lld:pubmed
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pubmed-article:7506046pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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