scholarly journals The Influence of Burst-Firing EMF on Forskolin-Induced Pheochromocytoma (PC12) Plasma Membrane Extensions

NeuroSci ◽  
2021 ◽  
Vol 2 (4) ◽  
pp. 383-399
Author(s):  
Trevor N. Carniello ◽  
Robert M. Lafrenie ◽  
Blake T. Dotta
Keyword(s):  
Plasma Membrane ◽  
Pc12 Cells ◽  
Electromagnetic Fields ◽  
Firing Pattern ◽  
Biological Function ◽  
Burst Firing ◽  
Intensity Pattern ◽  
Pheochromocytoma Pc12 ◽  
In Vitro Examination

Previous research has demonstrated that pheochromocytoma (PC12) cells treated with forskolin provides a model for the in vitro examination of neuritogenesis. Exposure to electromagnetic fields (EMFs), especially those which have been designed to mimic biological function, can influence the functions of various biological systems. We aimed to assess whether exposure of PC12 cells treated with forskolin to patterned EMF would produce more plasma membrane extensions (PME) as compared to PC12 cells treated with forskolin alone (i.e., no EMF exposure). In addition, we aimed to determine whether the differences observed between the proportion of PME of PC12 cells treated with forskolin and exposed to EMF were specific to the intensity, pattern, or timing of the applied EMF. Our results showed an overall increase in PME for PC12 cells treated with forskolin and exposed to Burst-firing EMF as compared to PC12 cells receiving forskolin alone. No other patterned EMF investigated were deemed to be effective. Furthermore, intensity and timing of the Burst-firing pattern did not significantly alter the proportion of PME of PC12 cells treated with forskolin and exposed to patterned EMF.

scholarly journals New Cyclic Diarylheptanoids from Platycarya strobilacea

Molecules ◽  
2020 ◽  
Vol 25 (24) ◽  
pp. 6034
Author(s):  
Wen-bing Ding ◽  
Rui-yuan Zhao ◽  
Guan-hua Li ◽  
Bing-lei Liu ◽  
Hua-liang He ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Pc12 Cells ◽  
Stem Bark ◽  
No Production ◽  
Electronic Circular Dichroism ◽  
Pheochromocytoma Pc12 ◽  
Pheochromocytoma Pc12 Cells ◽  
Induced Apoptosis ◽  
Circular Dichroïsm

Five new cyclic diarylheptanoids (platycary A–E, compounds 1–5) and three previously identified analogues (i.e., phttyearynol (compound 6), myricatomentogenin (compound 7), and juglanin D (compound 8)) were isolated from the stem bark of Platycarya strobilacea. The structures of these compounds were determined using NMR, HRESIMS, and electronic circular dichroism (ECD) data. The cytotoxicity of compounds 1–5 and their ability to inhibit nitric oxide (NO) production, as well as protect against the corticosterone-induced apoptosis of Pheochromocytoma (PC12) cells, were evaluated in vitro using the appropriate bioassays. Compounds 1 and 2 significantly inhibited the corticosterone-induced apoptosis of PC12 cells at a concentration of 20 μΜ.

scholarly journals Di-Leucine Signals Mediate Targeting of Tyrosinase and Synaptotagmin to Synaptic-like Microvesicles within PC12 Cells

1999 ◽  
Vol 10 (11) ◽  
pp. 3979-3990 ◽  
Author(s):  
Anastasiya D. Blagoveshchenskaya ◽  
Eric W. Hewitt ◽  
Daniel F. Cutler
Keyword(s):  
Plasma Membrane ◽  
Pc12 Cells ◽  
Brefeldin A ◽  
Adaptor Protein ◽  
Dependent Manner ◽  
Protein Traffic ◽  
C Terminus ◽  
Targeting Signal

One pathway in forming synaptic-like microvesicles (SLMV) involves direct budding from the plasma membrane, requires adaptor protein 2 (AP2) and is brefeldin A (BFA) resistant. A second route leads from the plasma membrane to an endosomal intermediate from which SLMV bud in a BFA-sensitive, AP3-dependent manner. Because AP3 has been shown to bind to a di-leucine targeting signal in vitro, we have investigated whether this major class of targeting signals is capable of directing protein traffic to SLMV in vivo. We have found that a di-leucine signal within the cytoplasmic tail of human tyrosinase is responsible for the majority of the targeting of HRP-tyrosinase chimeras to SLMV in PC12 cells. Furthermore, we have discovered that a Met-Leu di-hydrophobic motif within the extreme C terminus of synaptotagmin I supports 20% of the SLMV targeting of a CD4-synaptotagmin chimera. All of the traffic to the SLMV mediated by either di-Leu or Met-Leu is BFA sensitive, strongly suggesting a role for AP3 and possibly for an endosomal intermediate in this process. The differential reduction in SLMV targeting for HRP-tyrosinase and CD4-synaptotagmin chimeras by di-alanine substitutions or BFA treatment implies that different proteins use the two routes to the SLMV to differing extents.

Aminopeptidase B: a processing enzyme secreted and associated with the plasma membrane of rat pheochromocytoma (PC12) cells

1998 ◽  
Vol 111 (2) ◽  
pp. 161-169 ◽  
Author(s):  
A. Balogh ◽  
S. Cadel ◽  
T. Foulon ◽  
R. Picart ◽  
A. Der Garabedian ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Golgi Apparatus ◽  
Pc12 Cells ◽  
Culture Medium ◽  
Enzyme Secretion ◽  
Ionophore A23187 ◽  
Dependent Manner ◽  
Intact Cells ◽  
Pheochromocytoma Pc12 ◽  
Pheochromocytoma Pc12 Cells

Aminopeptidase B (Ap-B) is a Zn2+-dependent exopeptidase which selectively removes Arg and/or Lys residues from the N terminus of several peptide substrates. Isolated and characterized from rat testes, this ubiquitous enzyme may participate in the final stages of precursor processing mechanisms. To test this hypothesis, we have investigated the secretion and subcellular localization of this enzyme in a rat cell line of pheochromocytoma (PC12 cells). By using a combination of biochemical and immunocytochemical methods, the following observations were made: (i) the level of aminopeptidase B detectable in the cell culture medium increased with time; (ii) 8-bromo-adenosine 3′-5′-cyclic monophosphate and the Ca2+ ionophore A23187 both stimulated enzyme liberation in the culture medium; (iii) brefeldin A, an inhibitor of vesicular transport from the endoplasmic reticulum to the Golgi apparatus, decreased enzyme secretion in a time-dependent manner; (iv) whereas nocodazole, a microtubule depolymerizing agent, inhibited enzyme secretion, cytochalasin D, a microfilament disruption agent, had no effect on released aminopeptidase B level; (v) immunofluorescence demonstrated the presence of aminopeptidase B in the Golgi apparatus; (vi) immunofluorescence, electron microscopy and tests of enzyme activity on intact cells showed an association of the peptidase with the external face of the plasma membrane. Together these data strongly argued in favour of the enzyme secretion by PC12 cells. It is concluded that aminopeptidase B may participate in processing events occurring either during its intracellular transport along the secretory pathway or at the plasma membrane level, or both.

In vitro reinnervation of adult rat muscle fibres by foreign neurons and transformed chromaffin PC12 cells

1988 ◽  
Vol 234 (1274) ◽  
pp. 1-9 ◽  
Keyword(s):  
Pc12 Cells ◽  
Neuromuscular Junctions ◽  
Mean Amplitude ◽  
Muscle Fibres ◽  
Adult Rat ◽  
Rat Muscle ◽  
Pheochromocytoma Pc12 ◽  
Nerve Muscle ◽  
Miniature Endplate Potentials

Adult rat muscle fibres were dissociated by using collagenase and maintained in culture. One to nine days later, neurons obtained from stages 22–30 Xenopus laevis embryos, or neonatal spinal cord, or pheochromocytoma (PC12) cells treated with nerve growth factor were added. Subsequently, the co-cultures were maintained for up to eight days. Functional synapses were formed with variable efficiency: 12% in rat– Xenopus nerve–muscle co-cultures, 23% in rat–rat and 33% in PC12 co-cultures. Miniature endplate potentials(MEPPs) and currents (MEPCs) were recorded, at frequencies ranging from 0.01 to 0.9 Hz. Their mean amplitude was smaller than in normal mammalian muscles. The rise time and time-constant of decay of MEPCs was about seven to ten times longer than that found in the original muscle, resembling immature synapses. (+)-Tubocurarine abolished the MEPPs in the rat-PC12 neuromuscular junctions. It is concluded that dissociated adult rat muscle fibres retain their ability of being reinnervated, and can form functional synapses with foreign neurons and transformed chromaffin cells.

A Modeling Study Suggests Complementary Roles for GABAA and NMDA Receptors and the SK Channel in Regulating the Firing Pattern in Midbrain Dopamine Neurons

2004 ◽  
Vol 91 (1) ◽  
pp. 346-357 ◽  
Author(s):  
Alexander O. Komendantov ◽  
Olena G. Komendantova ◽  
Steven W. Johnson ◽  
Carmen C. Canavier
Keyword(s):  
Experimental Data ◽  
Firing Pattern ◽  
Receptor Activation ◽  
Burst Firing ◽  
Dopamine Neurons ◽  
Sk Channels ◽  
Sk Channel ◽  
The Difference

Midbrain dopaminergic (DA) neurons in vivo exhibit two major firing patterns: single-spike firing and burst firing. The firing pattern expressed is dependent on both the intrinsic properties of the neurons and their excitatory and inhibitory synaptic inputs. Experimental data suggest that the activation of N-methyl-d-aspartate (NMDA) and GABAA receptors is a crucial contributor to the initiation and suppression of burst firing, respectively, and that blocking Ca2+-activated potassium SK channels can facilitate burst firing. A multi-compartmental model of a DA neuron with a branching structure was developed and calibrated based on in vitro experimental data to explore the effects of different levels of activation of NMDA and GABAA receptors as well as the modulation of the SK current on the firing activity. The simulated tonic activation of GABAA receptors was calibrated by taking into account the difference in the electrotonic properties in vivo versus in vitro. Although NMDA-evoked currents are required for burst generation in the model, currents evoked by GABAA-receptor activation can also regulate the firing pattern. For example, the model predicts that increasing the level of NMDA receptor activation can produce excessive depolarization that prevents burst firing, but a concurrent increase in the activation of GABAA receptors can restore burst firing. Another prediction of the model is that blocking the SK channel current in vivo will facilitate bursting, but not as robustly as blocking the GABAA receptors.

scholarly journals Nerve growth factor-induced changes in the intracellular localization of the protein kinase C substrate B-50 in pheochromocytoma PC12 cells.

1989 ◽  
Vol 108 (3) ◽  
pp. 1115-1125 ◽  
Author(s):  
C O Van Hooff ◽  
J C Holthuis ◽  
A B Oestreicher ◽  
J Boonstra ◽  
P N De Graan ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Protein Kinase C ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Protein Kinase ◽  
Pc12 Cells ◽  
Plasma Membranes ◽  
Nerve Growth ◽  
Kinase C ◽  
Pheochromocytoma Pc12

High levels of the neuron-specific protein kinase C substrate, B-50 (= GAP43), are present in neurites and growth cones during neuronal development and regeneration. This suggests a hitherto nonelucidated role of this protein in neurite outgrowth. Comparable high levels of B-50 arise in the pheochromocytoma PC12 cell line during neurite formation. To get insight in the putative growth-associated function of B-50, we compared its ultrastructural localization in naive PC12 cells with its distribution in nerve growth factor (NGF)- or dibutyryl cyclic AMP (dbcAMP)-treated PC12 cells. B-50 immunogold labeling of cryosections of untreated PC12 cells is mainly associated with lysosomal structures, including multivesicular bodies, secondary lysosomes, and Golgi apparatus. The plasma membrane is virtually devoid of label. However, after 48-h NGF treatment of the cells, B-50 immunoreactivity is most pronounced on the plasma membrane. Highest B-50 immunoreactivity is observed on plasma membranes surrounding sprouting microvilli, lamellipodia, and filopodia. Outgrowing neurites are scattered with B-50 labeling, which is partially associated with chromaffin granules. In NGF-differentiated PC12 cells, B-50 immunoreactivity is, as in untreated cells, also associated with organelles of the lysosomal family and Golgi stacks. B-50 distribution in dbcAMP-differentiated cells closely resembles that in NGF-treated cells. The altered distribution of B-50 immunoreactivity induced by differentiating agents indicates a shift of the B-50 protein towards the plasma membrane. This translocation accompanies the acquisition of neuronal features of PC12 cells and points to a neurite growth-associated role for B-50, performed at the plasma membrane at the site of protrusion.

Toxic effect of zinc nanoscale metal-organic frameworks on rat pheochromocytoma (PC12) cells in vitro

2014 ◽  
Vol 271 ◽  
pp. 283-291 ◽  
Author(s):  
Fei Ren ◽  
Baochun Yang ◽  
Jing Cai ◽  
Yaodong Jiang ◽  
Jun Xu ◽  
...  
Keyword(s):  
Toxic Effect ◽  
Pc12 Cells ◽  
Metal Organic Frameworks ◽  
Metal Organic ◽  
Pheochromocytoma Pc12 ◽  
Pheochromocytoma Pc12 Cells

In Vitro Studies of Acrylamide Neurotoxicity in Rat Pheochromocytoma (PC12) Cells

1996 ◽  
Vol 24 (3) ◽  
pp. 359-366
Author(s):  
Weiquan W. Lin ◽  
Larry R. Johnson ◽  
Marvin A. Friedman ◽  
Mohamed B. Abou-Donia
Keyword(s):  
Protein Synthesis ◽  
Pc12 Cells ◽  
Molecular Mechanisms ◽  
Mrna Levels ◽  
Neurofilament Protein ◽  
Ngf Receptor ◽  
Pheochromocytoma Pc12 ◽  
Axonal Swellings

This review discusses our studies on molecular mechanisms of acrylamide neurotoxicity by using the rat pheochromocytoma (PC12) cell line. The results showed that: a) acrylamide altered the gross morphology of PC12 cells; b) acrylamide induced neurofilament accumulation in PC12 cells; c) the effects of acrylamide on PC12 cells are consistent with its neurotoxicity in vivo; d) acrylamide stimulated neurofilament protein synthesis in PC12 cells; e) acrylamide did not act via nerve growth factor (NGF) receptor gp140trk to regulate neurofilament synthesis in PC12 cells; f) dexamethasone antagonised NGF and/or acrylamide-induced neurofilament protein synthesis and expression; and g) acrylamide differentially regulated the mRNA levels of three neurofilament subunit genes in PC12 cells. These molecular studies provide the first evidence that: a) there are distinctive and convergent signalling pathways for NGF-regulated and acrylamide-regulated neurofilament expression; b) acrylamide may differentially regulate the expression of each subunit, resulting in aberrant accumulation of neurofilament proteins; and c) there is a dexamethasone-sensitive signalling step common to NGF and acrylamide. These results could partially explain the mechanisms of neurofilament accumulation in distal axonal swellings, a pathognomonic feature of acrylamide neurotoxicity.

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