scholarly journals Nerve growth factor affects Ca2+currents via the p75 receptor to enhance prolactin mRNA levels in GH3rat pituitary cells

2006 ◽  
Vol 574 (2) ◽  
pp. 349-365 ◽  
Author(s):  
Adriana M. López-Domínguez ◽  
Juan Luis Espinosa ◽  
Araceli Navarrete ◽  
Guillermo Avila ◽  
Gabriel Cota
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Pituitary Cells ◽  
Mrna Levels ◽  
Nerve Growth ◽  
P75 Receptor ◽  
Prolactin Mrna

Rescue of α-SNS Sodium Channel Expression in Small Dorsal Root Ganglion Neurons After Axotomy by Nerve Growth Factor In Vivo

1998 ◽  
Vol 79 (5) ◽  
pp. 2668-2676 ◽  
Author(s):  
S. D. Dib-Hajj ◽  
J. A. Black ◽  
T. R. Cummins ◽  
A. M. Kenney ◽  
J. D. Kocsis ◽  
...  
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Dorsal Root Ganglion ◽  
Sodium Channel ◽  
Dorsal Root ◽  
Sodium Current ◽  
Mrna Levels ◽  
Drg Neurons ◽  
Nerve Growth

Dib-Hajj, S. D., J. A. Black, T. R. Cummins, A. M. Kenney, J. D. Kocsis, and S. G. Waxman. Rescue of α-SNS sodium channel expression in small dorsal root ganglion neurons after axotomy by nerve growth factor in vivo. J. Neurophysiol. 79: 2668–2676, 1998. Small (18–25 μm diam) dorsal root ganglion (DRG) neurons are known to express high levels of tetrodotoxin-resistant (TTX-R) sodium current and the mRNA for the α-SNS sodium channel, which encodes a TTX-R channel when expressed in oocytes. These neurons also preferentially express the high affinity receptor for nerve growth factor (NGF), TrkA. Levels of TTX-R sodium current and of α-SNS mRNA are reduced in these cells after axotomy. To determine whether NGF participates in the regulation of TTX-R current and α-SNS mRNA in small DRG neurons in vivo, we axotomized small lumbar DRG neurons by sciatic nerve transection and administered NGF or Ringer solution to the proximal nerve stump using osmotic pumps. Ten to 12 days after pump implant, whole cell patch-clamp recording demonstrated that TTX-R current density was decreased in Ringer-treated axotomized neurons (154 ± 45 pA/pF; mean ± SE) compared with nonaxotomized control neurons (865 ± 123 pA/pF) and was restored partially toward control levels in NGF-treated axotomized neurons (465 ± 78 pA/pF). The V 1/2 for steady-state activation and inactivation of TTX-R currents were similar in control, Ringer- and NGF-treated axotomized neurons. Reverse transcription polymerase chain reaction revealed an upregulation of α-SNS mRNA levels in NGF-treated compared with Ringer-treated axotomized DRG. In situ hybridization showed that α-SNS mRNA levels were decreased significantly in small Ringer-treated axotomized DRG neurons in vivo and also in small DRG neurons that were dissociated and maintained in vitro, so as to correspond to the patch-clamp conditions. NGF-treated axotomized neurons had a significant increase in α-SNS mRNA expression, compared with Ringer-treated axotomized cells. These results show that the administration of exogenous NGF in vivo, to the proximal nerve stump of the transected sciatic nerve, results in an upregulation of TTX-R sodium current and of α-SNS mRNA levels in small DRG neurons. Retrogradely transported NGF thus appears to participate in the control of excitability in these cells via actions that include the regulation of sodium channel gene expression in vivo.

Short- and long-term mechanisms of tau regulation in PC12 cells

1995 ◽  
Vol 108 (8) ◽  
pp. 2857-2864 ◽  
Author(s):  
E. Sadot ◽  
J. Barg ◽  
D. Rasouly ◽  
P. Lazarovici ◽  
I. Ginzburg
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Pc12 Cells ◽  
Tau Protein ◽  
Immunoblot Analysis ◽  
Term Treatment ◽  
Mrna Levels ◽  
Short Term Treatment ◽  
Nerve Growth ◽  
Protein Levels

Induction by nerve growth factor of neurite outgrowth in PC12 cells is transcription-dependent and is associated with the accumulation of tau protein. It was recently shown that short-term treatment with staurosporine, a protein kinase alkaloid inhibitor, induced an elevation of tau protein levels and outgrowth of stable neurites. In this study, we analyzed the mechanism(s) by which nerve growth factor and staurosporine exert their effects on tau levels. We demonstrate that nerve growth factor affects tau mRNA stability, thus contributing to the observed increase in tau mRNA levels. On the other hand, tau mRNA levels were not affected by the treatment with staurosporine. We also demonstrate that the phosphorylation of tau protein was reduced after treatment of PC12 cells with nerve growth factor or staurosporine, as shown by immunoblot analysis using specific antibodies and alkaline phosphatase treatment. Thus, regulation of tau levels by nerve growth factor appears to be mediated by transcriptional, post-transcriptional and posttranslational steps, whereas the effect of staurosporine on tau levels may be attributed to its effect on the state of phosphorylation of the protein.

Effect of protein synthesis inhibitors on growth factor activation of c-fos, c-myc, and actin gene transcription

1986 ◽  
Vol 6 (4) ◽  
pp. 1050-1057
Author(s):  
M E Greenberg ◽  
A L Hermanowski ◽  
E B Ziff
Keyword(s):  
Protein Synthesis ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Pc12 Cells ◽  
Gene Transcription ◽  
Actin Gene ◽  
Mrna Levels ◽  
Protein Synthesis Inhibitors ◽  
3T3 Cells ◽  
Nerve Growth

Stimulation of quiescent 3T3 cells with purified growth factors or of the pheochromocytoma cell line PC12 with nerve growth factor results in the rapid transient induction of c-fos, c-myc, and actin gene transcription (M.E. Greenberg and E.B. Ziff, Nature [London] 312:711-716; M.E. Greenberg, L.A. Greene, and E.B. Ziff, J. Biol. Chem. 26:14101-14110). We used protein synthesis inhibitors to investigate whether synthesis of new proteins plays a role in the rapid induction and subsequent repression of the transcription of these genes. Pretreatment of quiescent 3T3 cells with the inhibitor anisomycin before growth factor stimulation caused a superinduction of c-fos and c-myc mRNA levels upon growth factor addition. Nuclear runoff transcription analyses of 3T3 cells indicated that anisomycin potentiated c-fos, c-myc, and also actin expression at the transcriptional level, possibly by inhibiting transcriptional repression. Somewhat different results were obtained when PC12 cells were incubated with either anisomycin or cycloheximide. In PC12 cells protein synthesis inhibitors superinduced nerve growth factor activation of c-fos mRNA production but completely abolished the activation of c-myc. The results suggest that in PC12 cells c-fos transcription is activated by a protein-synthesis-independent mechanism, whereas c-myc stimulation requires new protein synthesis. The difference in the effect of anisomycin on growth factor activation of c-myc expression in 3T3 versus PC12 cells may be due to differential stringency of protein synthesis inhibition in the two cells or could reflect cell type differences in c-myc regulation.

Effects of nerve crush and transection on mRNA levels for nerve growth factor receptor in the rat facial motoneurons

1991 ◽  
Vol 9 (1-2) ◽  
pp. 157-160 ◽  
Author(s):  
Takanori Saika ◽  
Emiko Senba ◽  
Koichi Noguchi ◽  
Makoto Sato ◽  
Shigetaka Yoshida ◽  
...  
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Growth Factor Receptor ◽  
Nerve Growth Factor Receptor ◽  
Mrna Levels ◽  
Nerve Crush ◽  
Nerve Growth ◽  
Facial Motoneurons
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