scholarly journals Cell motility affects the intensity of gap junctional coupling in prostate carcinoma and melanoma cell populations

1992 ◽  
Author(s):  
Jaroslaw Czyz
Keyword(s):  
Cell Motility ◽  
Melanoma Cell ◽  
Prostate Carcinoma ◽  
Cell Populations ◽  
Junctional Coupling ◽  
Gap Junctional ◽  
Gap Junctional Coupling

scholarly journals Apigenin inhibits growth and motility but increases gap junctional coupling intensity in rat prostate carcinoma (MAT-LyLu) cell populations

2008 ◽  
Vol 13 (3) ◽  
Author(s):  
Marta Czernik ◽  
Jolanta Sroka ◽  
Zbigniew Madeja ◽  
Jarosław Czyż
Keyword(s):  
Cell Proliferation ◽  
Cell Motility ◽  
Cell Model ◽  
Inhibitory Effect ◽  
Cancer Development ◽  
Junctional Coupling ◽  
Rat Prostate ◽  
Gap Junctional ◽  
Gap Junctional Coupling

AbstractApigenin (4′,5,7,-trihydroxyflavone) is a flavonoid abundant in the common fruits, herbs and vegetables constituting the bulk of the human diet. This study was aimed at quantifying the effects of apigenin on the basic cellular traits determining cancer development, i.e. cell proliferation, gap junctional coupling, and motility, using the Dunning rat prostate MAT-LyLu cell model. We demonstrated that apigenin considerably inhibits MAT-LyLu cell proliferation and significantly enhances the intensity of connexin43-mediated gap junctional coupling. This effect correlates with an increased abundance of C×43-positive plaques at the cell-to-cell borders seen in apigenin-treated variants. Moreover, we observed an inhibitory effect of apigenin on the motility of MAT-LyLu cells. The basic parameters characterising MAT-LyLu cell motility, especially the rate of cell displacement, considerably decreased upon apigenin administration. This in vitro data indicates that apigenin may affect cancer development in general, and prostate carcinogenesis in particular, via its influence on cellular activities decisive for both cancer promotion and progression, including cell proliferation, gap junctional coupling and cell motility and invasiveness.

Bursting in Inhibitory Interneuronal Networks: A Role for Gap-Junctional Coupling

1999 ◽  
Vol 81 (3) ◽  
pp. 1274-1283 ◽  
Author(s):  
F. K. Skinner ◽  
L. Zhang ◽  
J. L. Perez Velazquez ◽  
P. L. Carlen
Keyword(s):  
Theoretical Work ◽  
Oscillatory Behavior ◽  
Minimal Network ◽  
Junctional Coupling ◽  
Synchronization Mechanisms ◽  
The Individual ◽  
Gap Junctional ◽  
Gap Junctional Coupling ◽  
Inhibitory Networks

Bursting in inhibitory interneuronal networks: a role for gap-junctional coupling. Much work now emphasizes the concept that interneuronal networks play critical roles in generating synchronized, oscillatory behavior. Experimental work has shown that functional inhibitory networks alone can produce synchronized activity, and theoretical work has demonstrated how synchrony could occur in mutually inhibitory networks. Even though gap junctions are known to exist between interneurons, their role is far from clear. We present a mechanism by which synchronized bursting can be produced in a minimal network of mutually inhibitory and gap-junctionally coupled neurons. The bursting relies on the presence of persistent sodium and slowly inactivating potassium currents in the individual neurons. Both GABAA inhibitory currents and gap-junctional coupling are required for stable bursting behavior to be obtained. Typically, the role of gap-junctional coupling is focused on synchronization mechanisms. However, these results suggest that a possible role of gap-junctional coupling may lie in the generation and stabilization of bursting oscillatory behavior.

scholarly journals Short-term depression of gap junctional coupling in reticular thalamic neurons of absence epileptic rats

2016 ◽  
Vol 594 (19) ◽  
pp. 5695-5710 ◽  
Author(s):  
Denise Kohmann ◽  
Annika Lüttjohann ◽  
Thomas Seidenbecher ◽  
Philippe Coulon ◽  
Hans-Christian Pape
Keyword(s):  
Short Term ◽  
Thalamic Neurons ◽  
Junctional Coupling ◽  
Gap Junctional ◽  
Gap Junctional Coupling

Prolonged epileptiform bursting induced by 0-Mg2+ in rat hippocampal slices depends on gap junctional coupling

Neuroscience ◽  
2001 ◽  
Vol 105 (3) ◽  
pp. 579-587 ◽  
Author(s):  
R Köhling ◽  
S.J Gladwell ◽  
E Bracci ◽  
M Vreugdenhil ◽  
J.G.R Jefferys
Keyword(s):  
Hippocampal Slices ◽  
Junctional Coupling ◽  
Gap Junctional ◽  
Gap Junctional Coupling

scholarly journals Nerve Injury Induces Gap Junctional Coupling among Axotomized Adult Motor Neurons

2000 ◽  
Vol 20 (2) ◽  
pp. 674-684 ◽  
Author(s):  
Qiang Chang ◽  
Alberto Pereda ◽  
Martin J. Pinter ◽  
Rita J. Balice-Gordon
Keyword(s):  
Nerve Injury ◽  
Motor Neurons ◽  
Junctional Coupling ◽  
Gap Junctional ◽  
Gap Junctional Coupling

ATP-sensitive K+ channels (Kir6.1/SUR1) regulate gap junctional coupling in cochlear-supporting cells

2016 ◽  
Vol 468 (7) ◽  
pp. 1215-1222 ◽  
Author(s):  
Alexander Blödow ◽  
Daniela Begandt ◽  
Almke Bader ◽  
Annegret Becker ◽  
Alice Burghard ◽  
...  
Keyword(s):  
Supporting Cells ◽  
K Channels ◽  
Junctional Coupling ◽  
Cochlear Supporting Cells ◽  
Gap Junctional ◽  
Gap Junctional Coupling

Ca2+ regulation of gap junctional coupling in lens epithelial cells

2001 ◽  
Vol 281 (3) ◽  
pp. C972-C981 ◽  
Author(s):  
Grant C. Churchill ◽  
Monica M. Lurtz ◽  
Charles F. Louis
Keyword(s):  
Epithelial Cells ◽  
Gap Junctions ◽  
Direct Action ◽  
Hill Coefficient ◽  
Lens Epithelial Cells ◽  
Alexa Fluor ◽  
Agonist Stimulation ◽  
Junctional Coupling ◽  
Gap Junctional ◽  
Gap Junctional Coupling

The quantitative effects of Ca2+signaling on gap junctional coupling in lens epithelial cells have been determined using either the spread of Mn2+ that is imaged by its ability to quench the fluorescence of fura 2 or the spread of the fluorescent dye Alexa Fluor 594. Gap junctional coupling was unaffected by a mechanically stimulated cell-to-cell Ca2+wave. Furthermore, when cytosolic Ca2+ concentration (Ca[Formula: see text]) increased after the addition of the agonist ATP, coupling was unaffected during the period that Ca[Formula: see text] was maximal. However, coupling decreased transiently ∼5–10 min after agonist addition when Ca[Formula: see text] returned to resting levels, indicating that this transient decrease in coupling was unlikely due to a direct action of Ca[Formula: see text] on gap junctions. An increase in Ca[Formula: see text] mediated by the ionophore ionomycin that was sustained for several minutes resulted in a more rapid and sustained decrease in coupling (IC50 ∼300 nM Ca2+, Hill coefficient of 4), indicating that an increase in Ca[Formula: see text]alone could regulate gap junctions. Thus Ca[Formula: see text]increases that occurred during agonist stimulation and cell-to-cell Ca2+ waves were too transient to mediate a sustained uncoupling of lens epithelial cells.

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