scholarly journals Calcium influx into neurons can solely account for cell contact-dependent neurite outgrowth stimulated by transfected L1.

1992 ◽  
Vol 119 (4) ◽  
pp. 883-892 ◽  
Author(s):  
E J Williams ◽  
P Doherty ◽  
G Turner ◽  
R A Reid ◽  
J J Hemperly ◽  
...  
Keyword(s):  
Neurite Outgrowth ◽  
Pc12 Cells ◽  
Calcium Influx ◽  
Polysialic Acid ◽  
Cell Contact ◽  
3T3 Cells ◽  
Cerebellar Neurons ◽  
Calcium Dependent ◽  
Promote Neurite Outgrowth ◽  
Neural Cell Adhesion

We have used monolayers of control 3T3 cells and 3T3 cells expressing transfected human L1 as a culture substrate for rat PC12 cells and rat cerebellar neurons. PC12 cells and cerebellar neurons extended longer neurites on human L1 expressing cells. Neurons isolated from the cerebellum at postnatal day 9 responded equally as well as those isolated at postnatal day 1-4, and this contrasts with the failure of these older neurons to respond to the transfected human neural cell adhesion molecule (NCAM). Human L1-dependent neurite outgrowth could be blocked by antibodies that bound to rat L1 and, additionally, the response could be fully inhibited by pertussis toxin and substantially inhibited by antagonists of L- and N-type calcium channels. Calcium influx into neurons induced by K+ depolarization fully mimics the L1 response. Furthermore, we show that L1- and K+(-)dependent neurite outgrowth can be specifically inhibited by a reduction in extracellular calcium to 0.25 microM, and by pretreatment of cerebellar neurons with the intracellular calcium chelator BAPTA/AM. In contrast, the response was not inhibited by heparin or by removal of polysialic acid from neuronal NCAM both of which substantially inhibit NCAM-dependent neurite outgrowth. These data demonstrate that whereas NCAM and L1 promote neurite outgrowth via activation of a common CAM-specific second messenger pathway in neurons, neuronal responsiveness to NCAM and L1 is not coordinately regulated via posttranslational processing of NCAM. The fact that NCAM- and L1-dependent neurite outgrowth, but not adhesion, are calcium dependent provides further evidence that adhesion per se does not directly contribute to neurite outgrowth.

scholarly journals Ganglioside modulation of neural cell adhesion molecule and N-cadherin-dependent neurite outgrowth

1992 ◽  
Vol 117 (5) ◽  
pp. 1093-1099 ◽  
Author(s):  
P Doherty ◽  
SV Ashton ◽  
SD Skaper ◽  
A Leon ◽  
FS Walsh
Keyword(s):  
Cell Adhesion ◽  
Neurite Outgrowth ◽  
Pc12 Cells ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Neural Cell Adhesion Molecule ◽  
Calcium Influx ◽  
Neural Cell ◽  
3T3 Cells ◽  
Neural Cell Adhesion

We have used monolayers of control 3T3 cells and 3T3 cells expressing transfected human neural cell adhesion molecule (NCAM) or chick N-cadherin as a culture substrate for PC12 cells. NCAM and N-cadherin in the monolayer directly promote neurite outgrowth from PC12 cells via a G-protein-dependent activation of neuronal calcium channels. In the present study we show that ganglioside GM1 does not directly activate this pathway in PC12 cells. However, the presence of GM1 (12.5-100 micrograms/ml) in the co-culture was associated with a potentiation of NCAM and N-cadherin-dependent neurite outgrowth. Treatment of PC12 cells with GM1 (100 micrograms/ml) for 90 min led to trypsin-stable increases in both beta-cholera toxin binding to PC12 cells and an enhanced neurite outgrowth response to N-cadherin. The ganglioside response could be fully inhibited by treatment with pertussis toxin. These data are consistent with exogenous gangliosides enhancing neuritic growth by promoting cell adhesion molecule-induced calcium influx into neurons.

scholarly journals Stimulation of neurite outgrowth in PC12 cells by EGF and KCl depolarization: a Ca(2+)-independent phenomenon.

1995 ◽  
Vol 130 (3) ◽  
pp. 701-710 ◽  
Author(s):  
M D Mark ◽  
Y Liu ◽  
S T Wong ◽  
T R Hinds ◽  
D R Storm
Keyword(s):  
Map Kinase ◽  
Neurite Outgrowth ◽  
Pc12 Cells ◽  
Kinase Activity ◽  
Neurite Growth ◽  
Intracellular Camp ◽  
Regulation Of Transcription ◽  
Promote Neurite Outgrowth ◽  
Synergistic Regulation ◽  
Stimulation Of

MAP kinase activity is necessary for growth factor induction of neurite outgrowth in PC12 cells. Although NGF and EGF both stimulate MAP kinase activity, EGF does not stimulate neurite extension. We report that EGF, in combination with KCl, stimulates neurite outgrowth in PC12 cells. This phenomenon was independent of intracellular Ca2+ increases and not due to enhancement of MAP kinase activity over that seen with EGF alone. However, EGF plus KCl increased intracellular cAMP, and other cAMP elevating agents acted synergistically with EGF to promote neurite outgrowth. Stimulation of neurite outgrowth by cAMP and EGF was blocked by inhibitors of transcription suggesting that synergistic regulation of transcription by the cAMP and MAP kinase pathways may stimulate neurite growth.

Phytochemical constituents from Melicope pteleifolia that promote neurite outgrowth in PC12 cells

2016 ◽  
Vol 23 ◽  
pp. 565-572 ◽  
Author(s):  
Jing Xu ◽  
Xiaocong Sun ◽  
Xingyu Liu ◽  
Maoqin Peng ◽  
Shen Li ◽  
...  
Keyword(s):  
Neurite Outgrowth ◽  
Pc12 Cells ◽  
Promote Neurite Outgrowth ◽  
Phytochemical Constituents

scholarly journals Neural cell adhesion molecule regulates cell contact-mediated changes in choline acetyltransferase activity of embryonic chick sympathetic neurons

1988 ◽  
Vol 106 (2) ◽  
pp. 479-486 ◽  
Author(s):  
A Acheson ◽  
U Rutishauser
Keyword(s):  
Choline Acetyltransferase ◽  
Specific Activity ◽  
Ganglion Cells ◽  
Sympathetic Neurons ◽  
Polysialic Acid ◽  
Cell Contact ◽  
Adult Chicken ◽  
Fab Fragments ◽  
Neural Cell Adhesion ◽  
A Cell

E10 chick sympathetic ganglion cells display a cell contact-dependent rise in choline acetyltransferase (ChAT) specific activity over the first several days in culture. This effect can be mimicked by addition of crude membrane fractions prepared from E10 retina and adult chicken brain, but not by those from E10 brain. The effects of both cell-cell and membrane-cell contact are inhibited by the addition of anti-NCAM Fab fragments. The membranes capable of increasing ChAT and those which are ineffective all contain NCAM, however their relative levels of NCAM polysialic acid differ. Whereas membranes with high polysialic acid NCAM are ineffective, selective enzymatic removal of polysialic acid renders them capable of producing an increase in ChAT. The inhibition of NCAM-mediated adhesion produced by Fab fragments can be compensated for by addition of wheat germ agglutinin, but only with membranes whose NCAM has low levels of polysialic acid. Taken together, these data suggest that NCAM can regulate cell contact-mediated increases in ChAT activity. We propose that NCAM-mediated adhesion promotes contact between cell membranes to allow the transmission of an otherwise NCAM-independent signal. In addition, NCAM's polysialic acid moiety appears to influence the ability of cells to transmit this signal, even in the presence of an alternative adhesion mechanism.

scholarly journals Thy-1 antibody-triggered neurite outgrowth requires an influx of calcium into neurons via N- and L-type calcium channels

1993 ◽  
Vol 122 (1) ◽  
pp. 181-189 ◽  
Author(s):  
P Doherty ◽  
A Singh ◽  
G Rimon ◽  
SR Bolsover ◽  
FS Walsh
Keyword(s):  
Cell Adhesion ◽  
Calcium Channels ◽  
Neurite Outgrowth ◽  
Pc12 Cells ◽  
Adhesion Molecule ◽  
Pertussis Toxin ◽  
Cell Adhesion Molecule ◽  
Calcium Influx ◽  
Present Evidence ◽  
Cells Cultured

We present evidence that the neurite out-growth stimulated by the binding of Thy-1 antibodies to PC12 cells is mediated by calcium influx through both N- and L-type calcium channels. PC12 cells cultured on a noncellular substratum in the presence of NGF, or on a cellular substratum in the absence of NGF, responded to soluble Thy-1 antibody by extending longer neurites. The response required bivalent antibody and could be blocked by removing Thy-1 from the surface of PC12 cells with phosphatidylinositol specific phospholipase C. The response could also be blocked by reducing extracellular calcium to 0.25 mM, or by antagonists of L- and N-type calcium channels. Additionally, the response could be fully inhibited by preloading PC12 cells with BAPTA/AM which buffers changes in intracellular calcium. A heterotrimeric G-protein is also implicated in the pathway as the response could be fully inhibited by pertussis toxin. These data suggest that antibody-induced clustering of Thy-1 stimulates neurite outgrowth by activating a second messenger pathway that has previously been shown to underlie cell adhesion molecule (NCAM, N-cadherin, and L1), but not integrin or NGF-dependent neurite outgrowth.

scholarly journals Direct activation of second messenger pathways mimics cell adhesion molecule-dependent neurite outgrowth.

1992 ◽  
Vol 118 (3) ◽  
pp. 663-670 ◽  
Author(s):  
J L Saffell ◽  
F S Walsh ◽  
P Doherty
Keyword(s):  
Cell Adhesion ◽  
Protein Kinase ◽  
Calcium Channel ◽  
Neurite Outgrowth ◽  
Pc12 Cells ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Calcium Channel Antagonists ◽  
3T3 Cells ◽  
Second Messenger Pathways

We present evidence that direct activation of neuronal second messenger pathways in PC12 cells by opening voltage-dependent calcium channels mimics cell adhesion molecule (CAM)-induced differentiation of these cells. PC12 cells were cultured on monolayers of control 3T3 cells or 3T3 cells expressing transfected N-cadherin in the presence of KCl or a calcium channel agonist Bay K 8644. Both potassium depolarization and agonist-induced activation of calcium channels promoted substantial neurite outgrowth from PC12 cells cultured on control 3T3 monolayers and increased neurite outgrowth from those cultured on N-cadherin-expressing 3T3 monolayers. The potassium-induced response could be inhibited by L- and N-type calcium channel antagonists and by kinase inhibitor K-252b but was unaffected by pertussis toxin. In contrast activators of protein kinase C did not stimulate neurite outgrowth, and the neurite outgrowth response induced by activation of protein kinase A was not inhibited by calcium channel antagonists or pertussis toxin. These studies support the postulate that CAM-induced neuronal differentiation involves a specific transmembrane signaling pathway and suggest that activation of this pathway after CAM binding may be more important for the neurite outgrowth response than CAM-dependent adhesion per se.

Curcuminoids Promote Neurite Outgrowth in PC12 Cells through MAPK/ERK- and PKC-Dependent Pathways

2011 ◽  
Vol 60 (1) ◽  
pp. 433-443 ◽  
Author(s):  
Kuo-Kai Liao ◽  
Ming-Jiuan Wu ◽  
Pei-Yi Chen ◽  
Szu-Wei Huang ◽  
Shu-Jun Chiu ◽  
...  
Keyword(s):  
Neurite Outgrowth ◽  
Pc12 Cells ◽  
Promote Neurite Outgrowth
Sign in / Sign up

Export Citation Format

Share Document