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

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

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.

Increased Electrotonic Coupling in Spinal Motoneurons After Transient Botulinum Neurotoxin Paralysis in the Neonatal Rat

2003 ◽  
Vol 89 (2) ◽  
pp. 793-805 ◽  
Author(s):  
Angel M. Pastor ◽  
George Z. Mentis ◽  
Rosa R. De la Cruz ◽  
Eugenia Díaz ◽  
Roberto Navarrete
Keyword(s):  
Neuromuscular Transmission ◽  
Botulinum Neurotoxin ◽  
Maximum Amplitude ◽  
Neonatal Rat ◽  
Intracellular Recordings ◽  
Light Microscope Level ◽  
Electrotonic Coupling ◽  
Junctional Coupling ◽  
Gap Junctional ◽  
Gap Junctional Coupling

The effect of early postnatal blockade of neuromuscular transmission using botulinum neurotoxin (BoNT) type A on motoneuron gap junctional coupling was studied by means of intracellular recordings and biocytin labeling using the in vitro hemisected spinal cord preparation of neonatal rats. The somata of tibialis anterior (TA) motoneurons were retrogradely labeled at birth (P0) by intramuscular injection of fluorescent tracers. Two days later, BoNT was injected unilaterally into the TA muscle. The toxin blocked neuromuscular transmission for the period studied (P4–P7) as shown by tension recordings of the TA muscle. Retrograde horseradish peroxidase tracing in animals reared to adulthood demonstrated no significant cell death or changes in the soma size of BoNT-treated TA motoneurons. Intracellular recordings were carried out in prelabeled control and BoNT-treated TA motoneurons from P4 to P7. Graded stimulation of the ventral root at subthreshold intensities elicited short-latency depolarizing (SLD) potentials that consisted of several discrete components reflecting electrotonic coupling between two or more motoneurons. BoNT treatment produced a significant increase (67%) in the maximum amplitude of the SLD and in the number of SLD components as compared with control (3.1 ± 1.7 vs. 1.4 ± 0.7; means ± SD). The morphological correlates of electrotonic coupling were investigated at the light microscope level by studying the transfer of biocytin to other motoneurons and the putative sites of gap junctional interaction. The dye-coupled neurons clustered around the injected cell with close somato-somatic, dendro-somatic and -dendritic appositions that might represent the sites of electrotonic coupling. The size of the motoneuron cluster was, on average, 2.2 times larger after BoNT treatment. Our findings demonstrate that a short-lasting functional disconnection of motoneurons from their target muscle delays motoneuron maturation by halting the elimination of gap junctional coupling that normally occurs during early postnatal development.

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