scholarly journals Protein Kinase A-mediated Phosphorylation of Connexin36 in Mouse Retina Results in Decreased Gap Junctional Communication between AII Amacrine Cells

2006 ◽  
Vol 281 (44) ◽  
pp. 33163-33171 ◽  
Author(s):  
Stephanie Urschel ◽  
Thorsten Höher ◽  
Timm Schubert ◽  
Cantas Alev ◽  
Goran Söhl ◽  
...  
2018 ◽  
Vol 28 (17) ◽  
pp. 2739-2751.e3 ◽  
Author(s):  
Cole W. Graydon ◽  
Evan E. Lieberman ◽  
Nao Rho ◽  
Kevin L. Briggman ◽  
Joshua H. Singer ◽  
...  

2004 ◽  
Vol 315 (3) ◽  
pp. 407-412 ◽  
Author(s):  
Sung-Jin Park ◽  
Eun-Jin Lim ◽  
Su-Ja Oh ◽  
Jin-Woong Chung ◽  
Dennis W. Rickman ◽  
...  

2004 ◽  
Vol 167 (3) ◽  
pp. 555-562 ◽  
Author(s):  
Theresa S. Richards ◽  
Clarence A. Dunn ◽  
William G. Carter ◽  
Marcia L. Usui ◽  
John E. Olerud ◽  
...  

Phosphorylation of connexin43 (Cx43) on serine368 (S368) has been shown to decrease gap junctional communication via a reduction in unitary channel conductance. Examination of phosphoserine368 (pS368) in normal human skin tissue using a phosphorylation site–specific antibody showed relatively even distribution throughout the epidermal layers. However, 24 h after wounding, but not at 6 or 72 h, pS368 levels were dramatically increased in basal keratinocytes and essentially lost from suprabasal layers adjacent to the wound (i.e., within 200 μm of it). Scratch wounding of primary human keratinocytes caused a protein kinase C (PKC)-dependent increase in pS368 in cells adjacent to the scratch, with a time course similar to that found in the wounds. Keratinocytes at the edge of the scratch also transferred dye much less efficiently at 24 h, in a manner dependent on PKC. However, keratinocyte migration to fill the scratch required early (within <6 h) gap junctional communication. Our evidence indicates that PKC-dependent phosphorylation of Cx43 at S368 creates dynamic communication compartments that can temporally and spatially regulate wound healing.


2012 ◽  
Vol 107 (10) ◽  
pp. 2649-2659 ◽  
Author(s):  
A. Cyrus Arman ◽  
Alapakkam P. Sampath

The nervous system frequently integrates parallel streams of information to encode a broad range of stimulus strengths. In mammalian retina it is generally believed that signals generated by rod and cone photoreceptors converge onto cone bipolar cells prior to reaching the retinal output, the ganglion cells. Near absolute visual threshold a specialized mammalian retinal circuit, the rod bipolar pathway, pools signals from many rods and converges on depolarizing (AII) amacrine cells. However, whether subsequent signal flow to OFF ganglion cells requires OFF cone bipolar cells near visual threshold remains unclear. Glycinergic synapses between AII amacrine cells and OFF cone bipolar cells are believed to relay subsequently rod-driven signals to OFF ganglion cells. However, AII amacrine cells also make glycinergic synapses directly with OFF ganglion cells. To determine the route for signal flow near visual threshold, we measured the effect of the glycine receptor antagonist strychnine on response threshold in fully dark-adapted retinal cells. As shown previously, we found that response threshold for OFF ganglion cells was elevated by strychnine. Surprisingly, strychnine did not elevate response threshold in any subclass of OFF cone bipolar cell. Instead, in every OFF cone bipolar subclass strychnine suppressed tonic glycinergic inhibition without altering response threshold. Consistent with this lack of influence of strychnine, we found that the dominant input to OFF cone bipolar cells in darkness was excitatory and the response threshold of the excitatory input varied by subclass. Thus, in the dark-adapted mouse retina, the high absolute sensitivity of OFF ganglion cells cannot be explained by signal transmission through OFF cone bipolar cells.


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