Nerve growth factor , stimulated release

Gadient, R.A., Cron, K.C. and Otten, U. (1990) Interleukin-1 and tumor necrosis factor-alpha synergystically stimulate nerve growth factor (NGF) release from cultured rat astrocytes. Neurosci. Lett. 117 335-340. 

Figure 3.7 Schematic of stimulated nerve growth factor (NGF) release, (a) Voltage applied across the polymer in PBS solution causes the release of the biotin from the PPy surface. (b)A3V stimulation of the PPy showed an increase in theamountof NGF released from the surfaceofthe conductive poiymer. Short stimulations of 30 s did not result in as much release as long stimulations of 150 s. The asterisk indicates a statistical difference versus short stimulation, no stimulation and no biotin dopant (p <0.05) (Reprinted with permission from George, P. M., LaVan, D. A., Burdick, J. A. et al. Electrically Controlled Drug Delivery from Biotin-Doped Conductive Polypyrrole, Advanced Materials, 18, 5, 577-81. Copyright (2006) Wiley-VCH Verlag GmbH).

Saez ET, Pehar M, Vargas MR, Barbeito L, Maccioni RB (2006) Production of nerve growth factor by beta-amyloid-stimulated astrocytes induces p75NTR-dependent tau hyperphosphorylation in cultured hippocampal neurons. J Neurosci Res 84 1098-1106 Sala C, Roussignol G, Meldolesi J, Fagni L (2005) Key role of the postsynaptic density scaffold proteins Shank and Homer in the functional architecture of Ca homeostasis at dendritic spines in hippocampal neurons. J Neurosci 25 4587 592 Santello M, Volterra A (2008) Synaptic modulation by astrocytes via Ca(2-l-)-dependent glutamate release. Neuroscience 158 253-9... 

Like the estrogen levels, so the total testosterone level and the bioavailable testosterone level, in particular, decline in both sexes with age. Testosterone supplementation was reported to protect orchiectomized, aging male rats from osteoporosis (260), increase nerve growth factor levels in rat brain (261), or improve depression in aging men (262). The treatment of N2a cells and rat primary cere-brocortical neurons with testosterone increased secretion of sAPPa and diminished the release of A 3s (263). In a similar manner, treatment of GTl-7 rat hypothalamic cells with testosterone stimulated the a-secretory pathway by increasing the secretion of sAPPa, without affecting the total amount of cellular APP (216). In a group of six men treated for adenocarcinoma of the prostate with hormonal suppressants, the precipitous drop in their levels of testosterone and estradiol correlated with the increase of A/340 plasma levels (264). The therapeutic implications of observations like these remain uncertain. 

The main effect of inflammatory cells in nociception is to sensitize neurons. This occurs in the periphery when the immune response stimulates peripheral cells to secrete mediators that sensitize primary afferent neurons. Substances released by immune cells that sensitize nociceptors include histamine, serotonin, eicosanoids, interleukin 1, tumor necrosis factor-a, and nerve growth factor (Dray 1995 McMahon 1996 Tracey and Walker 1995). Sensitization also occurs in the CNS, and centrally located microglia, which express CB2Rs, may be involved in the sensitization of central nociceptive neurons during inflammation (reviewed by DeLeo et al. 2004). 

Abbreviations ACTH, adrenocorticotropic hormone BDNF. brain-derived neurotrophic factop I GI epidermal growth factop Epo, erythropoietin I SII follicle-stimulating hormone IGI -I insulin-like growth factor-I IL. interleukin NGF, nerve growth factop NT-3, neurotrophin-3 IGI -/fl Transforming growth factor-jSl ft 11 thyrotropin releasing hormone I SI I thyrotropin. Blockade of interleu-kin-2-dependent GPI hydrolysis. 

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