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

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.

Author(s):  
Jarosław Czyż

AbstractTumour development is a process resulting from the disturbance of various cellular functions including cell proliferation, adhesion and motility. While the role of these cell parameters in tumour promotion and progression has been widely recognized, the mechanisms that influence gap junctional coupling during tumorigenesis remain elusive. Neoplastic cells usually display decreased levels of connexin expression and/or gap junctional coupling. Thus, impaired intercellular communication via gap junctions may facilitate the release of a potentially neoplastic cell from the controlling regime of the surrounding tissue, leading to tumour promotion. However, recent data indicates that metastatic tumour cell lines are often characterized by relatively high levels of connexin expression and gap junctional coupling. This review outlines current knowledge on the role of connexins in tumorigenesis and the possible mechanisms of the interference of gap junctional coupling with the processes of tumour invasion and metastasis.


2007 ◽  
Vol 216 (1) ◽  
pp. 23-35 ◽  
Author(s):  
Lene Nygaard Axelsen ◽  
Ketil Haugan ◽  
Martin Stahlhut ◽  
Anne-Louise Kjølbye ◽  
James K. Hennan ◽  
...  

2013 ◽  
Vol 91 (2) ◽  
pp. 157-164 ◽  
Author(s):  
Dan Li ◽  
Poonampreet Sekhon ◽  
Kevin J. Barr ◽  
Lucrecia Márquez-Rosado ◽  
Paul D. Lampe ◽  
...  

Connexin43 has been recognized as forming gap junctions in Leydig cells. However, previous work has shown that mouse Leydig cells lacking this connexin do not suffer any limitation of their ability to produce testosterone when stimulated with luteinizing hormone. The objective of this study was to identify additional connexins in mouse Leydig cells that could be required for steroidogenesis. A reverse transcription – polymerase chain reaction screen involving isolated adult Leydig cells identified connexin36 and connexin45 as expressed along with connexin43. Treatment of dissociated testes with carbenoxolone, a nonspecific blocker of gap junctional coupling, significantly reduced testosterone output as did treatment with quinine, which disrupts coupling provided by connexin36 and connexin45 gap junctions but not those composed of connexin43, indicating that either or both of connexins 36 and 45 could be involved in supporting Leydig cell steroidogenesis. Immunolabeling of adult mouse testis sections confirmed the localization of connexin36 along with connexin43 in Leydig cell gap junctions but not connexin45, which is distributed throughout the cells. It was concluded that connexin36, connexin43, and connexin45 are coexpressed in Leydig cells with connexins 36 and 43 contributing to gap junctions. The role of connexin45 remains to be elucidated.


2006 ◽  
Vol 23 (2) ◽  
pp. 489-496 ◽  
Author(s):  
Éliane Proulx ◽  
Yevgen Leshchenko ◽  
Larisa Kokarovtseva ◽  
Vladislav Khokhotva ◽  
Mostafa El-Beheiry ◽  
...  

2016 ◽  
Vol 594 (19) ◽  
pp. 5695-5710 ◽  
Author(s):  
Denise Kohmann ◽  
Annika Lüttjohann ◽  
Thomas Seidenbecher ◽  
Philippe Coulon ◽  
Hans-Christian Pape

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

2000 ◽  
Vol 20 (2) ◽  
pp. 674-684 ◽  
Author(s):  
Qiang Chang ◽  
Alberto Pereda ◽  
Martin J. Pinter ◽  
Rita J. Balice-Gordon

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