Nerve growth factor inhibits sympathetic neurons’ response to an injury cytokine

Shadiack, Annette M.; Vaccariello, Stacey A.; Sun, Yi; Zigmond, Richard E.

doi:10.1073/pnas.95.13.7727

Cited by 41 publications

(32 citation statements)

References 29 publications

(27 reference statements)

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“…Sympathetic denervation could enhance pain transmission if sympathetic nerves and nociceptors competed for uptake or binding of neurotrophic factors. Acute sympathetic peripheral nerve damage increases expression of nerve growth factor in the dorsal root ganglion (47). Whether chronic sympathetic neuropathy alters expression of neurotrophic factors, augmenting pain sensation, is unknown.…”

Section: Discussionmentioning

confidence: 99%

Local Sympathetic Denervation in Painful Diabetic Neuropathy

et al. 2002

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This study assessed whether painful diabetic neuropathy is associated with abnormal sympathetic nervous function in the affected limbs. Nine patients with diabetes (four men, five women; age 61 ؎ 7 years) and painful peripheral neuropathy of the feet, but without evidence of generalized autonomic neuropathy, underwent intravenous infusion of tritiated norepinephrine (NE) and sampling of arterial and venous blood in both feet and in one arm to quantify the rate of entry of NE into the local venous plasma (NE spillover). In the same patients, positron emission tomography (PET) scanning after intravenous injection of the sympathoneural imaging agent 6-[18 F]fluorodopamine was used to visualize sympathetic innervation and after intravenous [13 N]ammonia to visualize local perfusion. The results were compared with those in the feet of normal volunteers and in an unaffected foot of patients with unilateral complex regional pain syndrome (CRPS). In addition, neurochemical results obtained in painful diabetic neuropathy were compared with those obtained in diabetic control patients with painless neuropathy and diabetic control patients without neuropathy. Local arteriovenous difference in plasma NE levels (⌬NE AV ) and NE spillover in the arms did not differ across the groups. However, ⌬NE AV in the feet was significantly less in the group with painful diabetic neuropathy than in the control groups. Also NE spillover in the feet tended to be lower in painful neuropathy. ⌬NE AV of diabetic control patients without neuropathy (n ‫؍‬ 6) resembled values in the control groups without diabetes, whereas patients with painless diabetic neuropathy (n ‫؍‬ 6) had evidence suggesting partial loss of sympathetic innervation. PET scanning revealed decreased flow-corrected 6-[18 F]fluorodopamine-derived radioactivity in patients with painful diabetic neuropathy, compared with values in normal volunteers and patients with CRPS. The results provide neurochemical and neuroimaging evidence for regionally selective sympathetic denervation in the painful feet of patients with diabetic neuropathy.

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Section: Discussionmentioning

confidence: 99%

Local Sympathetic Denervation in Painful Diabetic Neuropathy

et al. 2002

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“…These neurons are likely required to be available to occupy synaptic spaces vacated by dying mature cells so that olfactory function can be restored quickly (58,59). As mature neurons senesce and die, trophic factors are released, such as NGF (60), which antagonize the effects of LIF (61,62) and promote terminal differentiation. The fate of immature ORNs therefore depends on which signal prevails, in this case, either NGF or LIF.…”

Section: Discussionmentioning

confidence: 99%

Leukemia inhibitory factor inhibits neuronal terminal differentiation through STAT3 activation

Moon

Yoo

Matarazzo

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

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The discovery of stem cells in the adult central nervous system raises questions concerning the neurotrophic factors that regulate postnatal neuronal development. Olfactory receptor neurons (ORNs) are a useful model, because they are capable of robust neurogenesis throughout adulthood. We have investigated the role of leukemia inhibitory factor (LIF) in postnatal neuronal development by using ORNs as a model. LIF is a multifunctional cytokine implicated in various aspects of neuronal development, including phenotype determination, survival, and in response to nerve injury. LIF-deficient mice display significant increases, both in the absolute amount and in the number of cells expressing olfactory marker protein, a marker of mature ORNs. The maturation of ORNs was significantly inhibited by LIF in vitro. LIF activated the STAT3 pathway in ORNs, and transfection of ORNs with a dominant negative form of STAT3 abolished the effect of LIF. These findings demonstrate that LIF negatively regulates ORN maturation via the STAT3 pathway. Thus, LIF plays a critical role in controlling the transition of ORNs to maturity. Consequently, a population of ORNs is maintained in an immature state to facilitate the rapid repopulation of the olfactory epithelium with mature neurons during normal cell turnover or after injury.

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“…In sympathetic neurons, administration of antiserum to NGF (anti-NGF) to unoperated animals increases expression of galanin, vasoactive intestinal peptide, and activating transcription factor 3 (ATF3; Shadiack et al, 1998Shadiack et al, , 2001Hyatt Sachs et al, 2005) and decreases expression of neuropeptide Y, tyrosine hydroxylase, and the low affinity neurotrophin receptor p75 (Zhou and Rush, 1996;Shadiack et al, 2001;Hyatt Sachs et al, 2005). In sensory neurons, the changes produced by anti-NGF include increased expression of galanin, vasoactive intestinal peptide, c-jun, and damage-induced neuronal endopeptidase (Gold et al, 1993;Shadiack et al, 2001;Kato et al, 2002;Csillik et al, 2003) and decreased expression of substance P and calcitonin gene-related peptide (Shadiack et al, 2001).…”

Section: Introductionmentioning

confidence: 95%

Reduction in nerve growth factor availability leads to a conditioning lesion‐like effect in sympathetic neurons

et al. 2006

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Axotomized peripheral neurons are capable of regeneration, and the rate of regeneration can be enhanced by a conditioning lesion (i.e., a lesion prior to the lesion after which neurite outgrowth is measured). A possible signal that could trigger the conditioning lesion effect is the reduction in availability of a target-derived factor resulting from the disconnection of a neuron from its target tissue. We tested this hypothesis with respect to nerve growth factor (NGF) and sympathetic neurons by administering an antiserum to NGF to adult mice for 7 days prior to explantation or dissociation of the superior cervical ganglion (SCG) and subsequently measuring neurite outgrowth. The antiserum treatment dramatically lowered the concentration of NGF in the SCG and increased the rate of neurite outgrowth in both explants and cell cultures. The increase in neurite outgrowth was similar in magnitude to that seen after a conditioning lesion. To determine if exogenous NGF could block the effect of a conditioning lesion, mice were injected with NGF or cytochrome C immediately prior to unilateral axotomy of the SCG, and for 7 days thereafter. A conditioning lesion effect of similar magnitude was seen in NGF-treated and control animals. While NGF treatment increased NGF levels in the contralateral control ganglion, it did not significantly elevate levels in the axotomized ganglion. The results suggest that the decreased availability of NGF after axotomy is a sufficient stimulus to induce the conditioning lesion effect in sympathetic neurons. While NGF administration did not prevent the conditioning lesion effect, this may be due to the markedly decreased ability of sympathetic neurons to accumulate the growth factor after axotomy.

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Nerve growth factor inhibits sympathetic neurons’ response to an injury cytokine

Cited by 41 publications

References 29 publications

Local Sympathetic Denervation in Painful Diabetic Neuropathy

Local Sympathetic Denervation in Painful Diabetic Neuropathy

Leukemia inhibitory factor inhibits neuronal terminal differentiation through STAT3 activation

Reduction in nerve growth factor availability leads to a conditioning lesion‐like effect in sympathetic neurons

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