Immunology of nerve growth factor (NGF). The effect of NGF-antiserum on sensory ganglia in vitro

Development ◽  
1970 ◽  
Vol 23 (2) ◽  
pp. 273-287
Author(s):  
H. Hoffman
Keyword(s):  
Molecular Weight ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Sympathetic Ganglion ◽  
Sympathetic Ganglia ◽  
Sensory Ganglia ◽  
Nerve Growth ◽  
Adult Organism

The properties of the ‘Nerve Growth Factor’ (NGF) have been described extensively (Levi-Montalcini & Booker, 1960; Levi-Montalcini, 1965) and reviewed recently (Levi-Montalcini, 1966). This factor is a protein of molecular weight about 130000 in its aggregated form (Varon, Nomura & Shooter, 1967, 1968) but may be active in lower molecular weight forms (Cohen, 1959, 1960; Banks et al. 1968). It is widely distributed in the adult organism (Bueker, Schenkein & Bane, 1960) and exerts a controlling influence on the differentiation of sensory and sympathetic ganglia in developing chick embryos. In newborn mammals its administration influences sympathetic ganglion growth only. A possible role in the adult nervous system is suggested by Scott, Gutmann & Horsky (1966), who showed that injected NGF will increase protein synthesis in regenerating sensory neurons in vivo. Active proteins in complex biological systems may be removed in a highly selective fashion by specific antibodies which thus provide a valuable means of studying their action.

Regulation of N- and L-Type Ca2+ Channels in Adult Frog Sympathetic Ganglion B Cells by Nerve Growth Factor In Vitro and In Vivo

1997 ◽  
Vol 78 (6) ◽  
pp. 3359-3370 ◽  
Author(s):  
Saobo Lei ◽  
William F. Dryden ◽  
Peter A. Smith
Keyword(s):  
Nerve Growth Factor ◽  
B Cells ◽  
Growth Factor ◽  
Sympathetic Ganglion ◽  
Type I ◽  
Nerve Growth ◽  
Adult Frog ◽  
Adult Neuron

Lei, Saobo, William F. Dryden, and Peter A. Smith. Regulation of N- and L-type Ca2+ channels in adult frog sympathetic ganglion B cells by nerve growth factor in vitro and in vivo. J. Neurophysiol. 78: 3359–3370, 1997. To examine mechanisms responsible for the long-term regulation of Ca2+-channels in an adult neuron, changes in whole cell Ba2+ current ( I Ba) were examined in adult bullfrog sympathetic ganglion B cells in vitro. Cells were cultured at low density in defined, serum free medium. After 15 days, total I Ba was similar to the initial value, whereas I Ba density was reduced by ∼36%, presumably due to an increase in neuronal surface area. By contrast, I Ba density remained constant after 6–15 days in the presence of murine β-NGF (200 ng/ml), and total I Ba was almost doubled. Inclusion of cytosine arabinoside (Ara-C; 10 μM) to inhibit proliferation of nonneuronal cells, did not affect the survival of neurons in the absence of nerve growth factor (NGF) nor did it attenuate I Ba. Ara-C did not prevent the effect of NGF on I Ba. There were three independent components to the action of NGF; during 6–9 days, it increased ω-conotoxin-GVIA–sensitive N-type I Ba ( I Ba,N); increased nifedipine-sensitive L-type I Ba ( I Ba,L) and decreased inactivation of the total Ba2+ conductance ( g Ba). The latter effect involved a selective decrease in the amplitude of one of the four kinetic components that describe the inactivation process. Total I Ba was also 55.8% larger than control in the somata of B cells acutely dissociated from leopard frogs that had received prior subcutaneous injections of NGF. By contrast, injection of NGF antiserum decreased total I Ba by 29.4%. There was less inactivation of g Ba in B cells from NGF-injected animals than in cells from animals injected with NGF antiserum ( P < 0.001). These data suggest that NGF-like molecule(s) play(s) a role in the maintenance of I Ba in an adult amphibian sympathetic neuron; the presence of NGF may allow the neuron to maintain a constant relationship between cell size and current density. They also show that I Ba inactivation in an adult neuron can be modulated in a physiologically relevant way by an extracellular ligand.

Trophic regulation of action potential in bullfrog sympathetic neurones

1992 ◽  
Vol 70 (6) ◽  
pp. 826-834 ◽  
Author(s):  
Philip Traynor ◽  
William F. Dryden ◽  
Peter A. Smith
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Action Potential ◽  
Sympathetic Ganglion ◽  
Culture Medium ◽  
Retrograde Transport ◽  
Electrophysiological Response ◽  
Nerve Growth

These experiments tested the hypothesis that the normal electrophysiological properties of mature bullfrog sympathetic ganglion (BFSG) neurones are maintained by the retrograde supply of nerve growth factor-like molecules from peripheral target tissues. Maintenance of these cells in explant culture in the absence of nerve growth factor (NGF) for up to 30 days produced electrophysiological changes that resemble those previously shown to accompany axotomy in vivo. These included (i) an increase in action potential (ap) duration (spike width), (ii) a decrease in the amplitude of the afterhyperpolarization (ahp), which follows the ap, and (iii) a rapidly developing decrease in ahp duration. When murine NGF (2.5 s; 50 ng/mL) was included in the culture medium there was less attentuation of ahp amplitude. Inclusion of affinity-isolated sheep lgG antibodies (0.5 μg/mL; raised against murine 2.5 s NGF) in the culture medium promoted a greater reduction in ahp amplitude than was seen in the "control" explants that were maintained in the absence of NGF. By contrast, the decrease in ahp duration that occurred in control explants was neither attenuated by exposure to NGF nor was it enhanced by NGF antibodies. Also, the increase in spike width that was seen in control explants was enhanced both by murine NGF and by NGF antibodies. Although some of the data support the hypothesis that factor(s) with some similarity to NGF may be synthesized by BFSG in vitro, loss of the retrograde transport of such factors does not explain all aspects of the electrophysiological response to target deprivation and (or) axotomy.Key words: sympathetic ganglion, axotomy, tissue culture, action potential afterhyperpolarization, nerve growth factor.

scholarly journals Gangliosides potentiate in vivo and in vitro effects of nerve growth factor on central cholinergic neurons.

1989 ◽  
Vol 86 (6) ◽  
pp. 2056-2060 ◽  
Author(s):  
A. C. Cuello ◽  
L. Garofalo ◽  
R. L. Kenigsberg ◽  
D. Maysinger
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Cholinergic Neurons ◽  
Nerve Growth ◽  
In Vitro Effects

scholarly journals Cartilage injury regulates nerve growth factor (NGF) in vitro and in vivo and drives painful behaviour in murine OA

2014 ◽  
Vol 22 ◽  
pp. S35
Author(s):  
C. Driscoll ◽  
A. Chanalaris ◽  
C. Knight ◽  
C. Gentry ◽  
S. Bevan ◽  
...  
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Cartilage Injury ◽  
Nerve Growth

The in vitro effect of the nerve growth factor on chick embryo spinal ganglia—a light-microscopic evaluation

Development ◽  
1970 ◽  
Vol 24 (2) ◽  
pp. 381-392
Author(s):  
Peddrick Weis
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Chick Embryo ◽  
Culture Period ◽  
Spinal Ganglia ◽  
Nerve Growth ◽  
Microscopic Evaluation ◽  
Vitro Effect

The effect of the nerve growth factor (NGF) on chick embryo spinal ganglia was studied in the hanging-drop bioassay system by comparison with parallel development in vivo. The well-differentiated ventrolateral neuroblasts, which in vivo increase 1·33 times in size during the culture period, did not increase in size at all in vitro. Only 65–72% survived to the end of the culture period regardless of the NGF concentration. The less-differentiated mediodorsal (M-D) neuroblasts, which in vivo increase 1·31 times in size during the culture period, were found to increase equally in vitro if sufficient NGF was present. Such a quantity was greater than that which evoked maximum outgrowth of neurites. Survival of M-D neuroblasts was also related to NGF concentration but did not equal the in vivo condition even at the highest concentration. The hyperchromatic type of degeneration prevented by high NGF concentrations is that which results in vivo from insufficient peripheral field. From this and other reports it would appear that the response to NGF seen in vitro is due only to the M-D neuroblasts, and that all biochemical and cytological observations which have been reported would therefore represent conditions within those cells only.

scholarly journals MicroRNA-98 reduces nerve growth factor expression in nicotine-induced airway remodeling

2020 ◽  
Vol 295 (52) ◽  
pp. 18051-18064
Author(s):  
Cherry Wongtrakool ◽  
Junsuk Ko ◽  
Andrew J. Jang ◽  
Kora Grooms ◽  
Sarah Chang ◽  
...  
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Airway Remodeling ◽  
Luciferase Reporter ◽  
Mouse Lung ◽  
Luciferase Expression ◽  
Nerve Growth ◽  
Pparγ Agonist

Evolving evidence suggests that nicotine may contribute to impaired asthma control by stimulating expression of nerve growth factor (NGF), a neurotrophin associated with airway remodeling and airway hyperresponsiveness. We explored the hypothesis that nicotine increases NGF by reducing lung fibroblast (LF) microRNA-98 (miR-98) and PPARγ levels, thus promoting airway remodeling. Levels of NGF, miR-98, PPARγ, fibronectin 1 (FN1), endothelin-1 (EDN1, herein referred to as ET-1), and collagen (COL1A1 and COL3A1) were measured in human LFs isolated from smoking donors, in mouse primary LFs exposed to nicotine (50 μg/ml), and in whole lung homogenates from mice chronically exposed to nicotine (100 μg/ml) in the drinking water. In selected studies, these pathways were manipulated in LFs with miR-98 inhibitor (anti-miR-98), miR-98 overexpression (miR-98 mimic), or the PPARγ agonist rosiglitazone. Compared with unexposed controls, nicotine increased NGF, FN1, ET-1, COL1A1, and COL3A1 expression in human and mouse LFs and mouse lung homogenates. In contrast, nicotine reduced miR-98 levels in LFs in vitro and in lung homogenates in vivo. Treatment with anti-miR-98 alone was sufficient to recapitulate increases in NGF, FN1, and ET-1, whereas treatment with a miR-98 mimic significantly suppressed luciferase expression in cells transfected with a luciferase reporter linked to the putative seed sequence in the NGF 3′UTR and also abrogated nicotine-induced increases in NGF, FN1, and ET-1 in LFs. Similarly, rosiglitazone increased miR-98 and reversed nicotine-induced increases in NGF, FN1, and ET-1. Taken together, these findings demonstrate that nicotine-induced increases in NGF and other markers of airway remodeling are negatively regulated by miR-98.

scholarly journals Recombinant human nerve growth factor with a marked activity in vitro and in vivo

2005 ◽  
Vol 102 (51) ◽  
pp. 18658-18663 ◽  
Author(s):  
A. M. Colangelo ◽  
N. Finotti ◽  
M. Ceriani ◽  
L. Alberghina ◽  
E. Martegani ◽  
...  
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Nerve Growth ◽  
Marked Activity ◽  
Human Nerve

991 Nerve growth factor released from the bladder in-vitro and in-vivo: Effect of bladder outlet obstruction and α1-blocker

2012 ◽  
Vol 11 (1) ◽  
pp. e991-e991a
Author(s):  
H. Akino ◽  
K. Nagase ◽  
N. Watanabe ◽  
K. Tanase ◽  
H. Ito ◽  
...  
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Bladder Outlet Obstruction ◽  
Outlet Obstruction ◽  
Nerve Growth ◽  
Α1 Blocker
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