Differential regulation of neurotrophin expression by mitogens and neurotransmitters in mouse lymphocytes

Barouch, Rina; Appel, Elena; Kazimirsky, Gila; Braun, Armin; Renz, Harald; Brodie, Chaya

doi:10.1016/s0165-5728(99)00233-7

Cited by 71 publications

(38 citation statements)

References 50 publications

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“…In the injured nerves, NGF produced by inflammatory cells such as macrophages and lymphocytes is increased. 8,[12][13][14] NGF increases in human neuroma, 46 so the environment around the nerve at the time of injury, such as bleeding or scarring by trauma, probably plays an important role in the increase in NGF or neuropathic pain. If NGF is subcutaneously injected into humans, deep pain such as muscle pain occurs, 22 and if administered to rodents, hyperesthesia occurs.…”

Section: Discussionmentioning

confidence: 99%

“…8,[12][13][14] NGF is a factor associated with development and regeneration of nerve tissue, and is involved in the occurrence of pain. 15,16 NGF itself not only acts as an algesic substance, but also binds to the NGF receptor TrkA, which is taken into the nociceptive fibers and transferred to the cell body of the dorsal root ganglion (DRG) via retrograde axonal transport to regulate gene expression related to pain.…”

Section: Introductionmentioning

confidence: 99%

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The autotomy relief effect of a silicone tube covering the proximal nerve stump

et al. 2006

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A technique of covering the proximal nerve stump (PNS) has been reported as a preventative method or treatment for neuroma. However, its detailed pain relief mechanism remains unknown. We created a silicone tube model in which the PNS of the rat sciatic nerve was introduced into the tube, whereas the controls had no tube. The score of autotomy observed in the tube group was lower than that in the control group at 3 days to 2 weeks after surgery, which suggested that the silicone tube had pain-like behavior inhibitory action. To elucidate the mechanism of autotomy inhibition, immunohistochemistry and Toluidine blue staining were performed in the PNS. The increase in S-100-immunoreactivity (IR) including Schwann cells was inhibited at 1 week after surgery in the tube group, and the increase in the number of macrophages shown by ED-1-IR at 1, 2, and 4 weeks after surgery was similarly inhibited. Toluidine blue staining showed that the increase in the number of mast cells was inhibited at 1, 2, and 4 weeks after surgery and in the number of lymphocytes at 1 and 2 weeks after surgery in the tube group. Therefore, blocking of the infiltration of inflammatory cells into the PNS by the silicone tube was thought to be the mechanism of autotomy inhibition. To further explore details of this mechanism, the expression of nerve growth factor (NGF), production of which is induced by inflammatory cells and of the NGF receptor TrkA was examined in the PNS and the dorsal root ganglion using immunohistochemistry and a ribonuclease protection assay. In the PNS, the increase in NGF-IR was inhibited at 1, 2, and 4 weeks after surgery in the tube group, suggesting that this could be one of the pain-like behavior inhibitory effects. ß

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The autotomy relief effect of a silicone tube covering the proximal nerve stump

et al. 2006

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“…A known source of NT-3 in human airways are eosinophils (Barouch et al, 2000;Kobayashi et al, 2002), whereas BDNF can be derived from macrophages, T-lymphocytes and epithelial cells (Barouch et al, 2000;Braun et al, 1999;Kerschensteiner et al, 1999). However, whether NT-3 or BDNF affects the neural activity and contribute to AHR is not clear (Renz, 2001).…”

Section: Introductionmentioning

confidence: 99%

Prolonged exposure to NT-3 attenuates cholinergic nerve-mediated contractions in cultured murine airways

Bachar

Adner

Uddman

et al. 2005

Respiratory Physiology & Neurobiology

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Prolonged exposure to NT-3 attenuates cholinergic nerve-mediated contractions in cultured murine airways.Bachar, Ofir; Adner, Mikael; Uddman, Rolf; Cardell, Lars-Olaf General rights Copyright and moral rights for the publications made accessible in the public portal are retained by the authors and/or other copyright owners and it is a condition of accessing publications that users recognise and abide by the legal requirements associated with these rights.• Users may download and print one copy of any publication from the public portal for the purpose of private study or research.• You may not further distribute the material or use it for any profit-making activity or commercial gain • You may freely distribute the URL identifying the publication in the public portal AbstractChronic airway inflammation may induce subsequent airway hyperresponsiveness (AHR) including pathological alteration of neural activity. Asthmatic airways contain elevated levels of neurotrophin-3 (NT-3) and brain-derived neurotrophic factor (BDNF) albeit; their effect on neural activity is unclear. This study evaluates the effects of NT-3 and BDNF on nerve mediated airway contractions in-vitro. Tracheal segments from BALB/c mice were cultured for 4 days with NT-3 or BDNF. Responsiveness to electric field stimulation (EFS) was evaluated in organ-bath and innervation patterns were examined by quantitative immunohistochemistry. In cultured segments the EFS induced contractions were inhibited by tetrodotoxin or atropine. NT-3 reduced the EFS contractions in a concentration-dependent manner whereas BDNF had no effect. The amount of nerve fibers, found in conjunction with the tracheal smooth muscle, was similar in NT-3 treated and control segments. In conclusion, NT-3 attenuates cholinergic nerve-mediated contractions of airway in-vitro. Considering the elevated levels of NT-3 found in asthmatic airways, the findings imply a protective role of NT-3 in AHR.

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“…In addition to neurons, non-neuronal cells such as mast cells (Leon et al, 1994), ®broblasts (Hattori et al, 1994), T-cells (Lambiase et al, 1997;Moalem et al, 2000), eosinophils (Solomon et al, 1998) and lymphocytes (Barouch et al, 2000) are able to synthesize NGF. NGF shows various pathologic properties in in¯ammatory models, which could be interesting in relation to allergic asthma as well (reviewed in Braun et al, 1999;2000).…”

Section: Introductionmentioning

confidence: 99%

The role of sensory nerve endings in nerve growth factor‐induced airway hyperresponsiveness to histamine in guinea‐pigs

Vries

Rijnsoever

Engels

et al. 2001

British J Pharmacology

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1 Nerve growth factor induces an airway hyperresponsiveness in vivo in guinea-pigs, as we have shown previously. Since antagonizing the neurokinin-1 (NK 1 ) receptor can prevent this NGFinduced airway hyperresponsiveness and since sensory nerves release tachykinins, we investigated the role of sensory nerves in the NGF-induced airway hyperresponsiveness. 2 We used isolated tracheal rings from guinea-pigs to measure tracheal contractility. In these rings sensory nerve endings are present, but these endings lack any contact with their cell bodies. 3 In this in vitro system, NGF dose-dependently induced a tracheal hyperresponsiveness to histamine. The NK 1 receptor antagonist SR140333 could block the induction of tracheal hyperresponsiveness. 4 To further investigate the involvement of sensory nerve endings we used the cannabinoid receptor 1 (CB 1 ) agonist R-methanandamide to inhibit excitatory events at the nerve terminal. The CB 1 receptor agonist was capable of blocking the tracheal hyperresponsiveness to NGF in the isolated system, as well as the airway hyperresponsiveness to NGF in vivo. 5 This indicates that NGF can induce an increase in airway responsiveness in the absence of sensory nerve cell bodies. NGF may act by increasing substance P release from sensory nerve endings, without upregulation of substance P in the neurons. Substance P in its turn is responsible for the induction of the NGF-induced airway hyperresponsiveness.

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Differential regulation of neurotrophin expression by mitogens and neurotransmitters in mouse lymphocytes

Cited by 71 publications

References 50 publications

The autotomy relief effect of a silicone tube covering the proximal nerve stump

The autotomy relief effect of a silicone tube covering the proximal nerve stump

Prolonged exposure to NT-3 attenuates cholinergic nerve-mediated contractions in cultured murine airways

The role of sensory nerve endings in nerve growth factor‐induced airway hyperresponsiveness to histamine in guinea‐pigs

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