Intercellular communication in sensory ganglia by purinergic receptors and gap junctions: Implications for chronic pain

2012 ◽  
Vol 1487 ◽  
pp. 183-191 ◽  
Author(s):  
Menachem Hanani
Keyword(s):  
Chronic Pain ◽  
Gap Junctions ◽  
Intercellular Communication ◽  
Purinergic Receptors ◽  
Sensory Ganglia

scholarly journals Intercellular calcium signalling between chondrocytes and synovial cells in co-culture

1998 ◽  
Vol 329 (3) ◽  
pp. 681-687 ◽  
Author(s):  
Paola D'ANDREA ◽  
Alessandra CALABRESE ◽  
Micaela GRANDOLFO
Keyword(s):  
Gap Junctions ◽  
Intercellular Communication ◽  
Structural Changes ◽  
Articular Chondrocytes ◽  
Cell Metabolism ◽  
Second Messengers ◽  
Calcium Signalling ◽  
Cell Types ◽  
Synovial Cells ◽  
Cell Coupling

Intercellular communication allows the co-ordination of cell metabolism between tissues as well as sensitivity to extracellular stimuli. Paracrine stimulation and cell-to-cell coupling through gap junctions induce the formation of complex cellular networks that favour the intercellular exchange of nutrients and second messengers. Heterologous intercellular communication was studied in co-cultures of articular chondrocytes and HIG-82 synovial cells by measuring mechanically induced cytosolic changes in Ca2+ ion levels by digital fluorescence video imaging. In confluent co-cultures, mechanical stimulation induced intercellular Ca2+ waves that propagated to both cell types with similar kinetics. Intercellular wave spreading was inhibited by 18α-glycyrrhetinic acid and by treatments inhibiting the activation of purinoreceptors, suggesting that intercellular signalling between these two cell types occurs both through gap junctions and ATP-mediated paracrine stimulation. In rheumatoid arthritis the formation of the synovial pannus induces structural changes at the chondrosynovial junction, where chondrocyte and synovial cells come into close apposition: these results provide the first evidence for direct intercellular communication between these two cell types.

scholarly journals Low pH enhances connexin32 degradation in the pancreatic acinar cell

2014 ◽  
Vol 307 (1) ◽  
pp. G24-G32 ◽  
Author(s):  
Anamika M. Reed ◽  
Thomas Kolodecik ◽  
Sohail Z. Husain ◽  
Fred S. Gorelick
Keyword(s):  
Gap Junctions ◽  
Acinar Cell ◽  
Intercellular Communication ◽  
Pancreatic Acinar Cell ◽  
Low Ph ◽  
Extracellular Ph ◽  
Gap Junctional Intercellular Communication ◽  
Junction Protein ◽  
Clinical Conditions ◽  
Gap Junctional

Decreased extracellular pH is observed in a number of clinical conditions and can sensitize to the development and worsen the severity of acute pancreatitis. Because intercellular communication through gap junctions is pH-sensitive and modulates pancreatitis responses, we evaluated the effects of low pH on gap junctions in the rat pancreatic acinar cell. Decreasing extracellular pH from 7.4 to 7.0 significantly inhibited gap junctional intracellular communication. Acidic pH also significantly reduced levels of connexin32, the predominant gap junction protein in acinar cells, and altered its localization. Increased degradation through the proteasomal, lysosomal, and autophagic pathways mediated the decrease in connexin32 under low-pH conditions. These findings provide the first evidence that low extracellular pH can regulate gap junctional intercellular communication by enhancing connexin degradation.

Increased Intercellular Communication through Gap Junctions May Contribute to Progression of Osteoarthritis

2004 ◽  
Vol 422 ◽  
pp. 224-232 ◽  
Author(s):  
Andrew A Marino ◽  
David D Waddell ◽  
Oleg V Kolomytkin ◽  
William D Meek ◽  
Robert Wolf ◽  
...  
Keyword(s):  
Gap Junctions ◽  
Intercellular Communication

Neuroimmune Interactions and Pain

2019 ◽  
pp. 363-387
Author(s):  
Jiahe Li ◽  
Peter M. Grace
Keyword(s):  
Chronic Pain ◽  
Neuropathic Pain ◽  
Nerve Injury ◽  
Purinergic Receptors ◽  
Critical Role ◽  
Oxygen Species ◽  
Neuroimmune Interactions ◽  
Sphingosine 1 Phosphate ◽  
Necrosis Factor

Chronic pain imposes a tremendous burden on the sufferer’s quality of life. Mounting evidence supports a critical role for neuroimmune interactions in the development and maintenance of chronic pain. Nerve injury leads to the activation of glia via sphingosine-1-phosphate, Toll-like receptors, chemokines, neuropeptides, and purinergic receptors. In turn, activated glia influence neuronal activity via interleukin 1β, tumor necrosis factor, brain-derived neurotrophic factor, reactive oxygen species, and excitatory amino acids. Epigenetic mechanisms of neuroimmune communication are also discussed. Investigation of neuroimmune interactions after peripheral nerve injury broadens our understanding of the mechanisms that drive neuropathic pain, and such interactions provide potential therapeutic targets for managing neuropathic pain.

scholarly journals Intercellular communication in normal and regenerating rat liver: a quantitative analysis.

1981 ◽  
Vol 91 (2) ◽  
pp. 505-523 ◽  
Author(s):  
D J Meyer ◽  
S B Yancey ◽  
J P Revel
Keyword(s):  
Gap Junctions ◽  
Intercellular Communication ◽  
Current Flow ◽  
Freeze Fracture ◽  
Normal Liver ◽  
Physiological Data ◽  
Regenerating Liver ◽  
Weanling Rats ◽  
Electrophysiological Studies ◽  
Intercellular Spread

We have compared intercellular communication in the regenerating and normal livers of weanling rats. The electrophysiological studies were conducted at the edge of the liver, and we have found that here as elsewhere in the liver there is a dramatic decrease in the number and size of gap junctions during regeneration. The area of hepatocyte membrane occupied by gap junctions is reduced 100-fold 29-35 h after hepatectomy. By combining observations made with the scanning electron microscope with our freeze fracture data we have estimated the number of "communicating interfaces" (areas of contact between hepatocytes that include at least one gap junction) formed by hepatocytes in normal and regenerating liver. In normal liver a hepatocyte forms gap junctions with every hepatocyte it contacts (approximately 6). In regenerating liver a hepatocyte forms detectable gap junctions with, on average, only one other hepatocyte. Intercellular spread of fluorescent dye and electric current is reduced in regenerating as compared with normal liver. The incidence of electric coupling is reduced from 100% of hepatocyte pairs tested in control liver to 92% in regenerating liver. Analysis of the spatial dependence of electronic potentials indicates a substantial increase in intercellular resistance in regenerating liver. A quantitative comparison of our morphological and physiological data is complicated by tortuous pattern of current flow and by inhomogeneities in the liver during regeneration. Nevertheless we believe that our results are consistent with the hypothesis that gap junctions are aggregates of channels between cell interiors.

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