Adenylate cyclase and carbonic anhydrase in the semicircular canal epithelium of the frog Rana esculenta

1990 ◽  
Vol 262 (3) ◽  
pp. 579-585 ◽  
Author(s):  
Olivier Oudar ◽  
Evelyne Ferrary ◽  
G�rard Feldmann
1991 ◽  
Vol 111 (2) ◽  
pp. 281-285 ◽  
Author(s):  
Evelyne Ferrary ◽  
Olivier Oudar ◽  
Christian Bernard ◽  
Gérard Friedlander ◽  
Gérard Feldmann ◽  
...  

1980 ◽  
Vol 185 (2) ◽  
pp. 373-383 ◽  
Author(s):  
Victor S. Sapirstein ◽  
Cheryl Flynn ◽  
Marjorie B. Lees

1986 ◽  
Vol 371 (1) ◽  
pp. 17-28 ◽  
Author(s):  
C Bernard ◽  
E Ferrary ◽  
O Sterkers

2008 ◽  
Vol 18 (2-3) ◽  
pp. 89-96
Author(s):  
Paolo Valli ◽  
Laura Botta ◽  
Gianpiero Zucca ◽  
Stefano Valli ◽  
Angelo Buizza

The physical mechanisms responsible for cupulolithiasis and canalolithiasis have been investigated by two groups of experiments in isolated posterior semicircular canal (SCC) of frog (Rana esculenta L.). First, clouds of 10-30 isolated otoconia were let to fall (snowfall of otoconia) either through the ampulla onto the cupula, or inside the long arm of the canal, opposite to the cupula. Second, microspheres ranging 30 to 350 μm in diameter were gently moved to and fro inside the long arm of the canal by a micromanipulator. The effects were evaluated by recording the firing rate (Nfr) of the ampullary nerve. Snowfall of otoconia produced detectable changes of Nfr only when otoconia got in contact with the cupula, but not when falling through the endolymph. Movement of the microspheres in the canal long arm induced Nfr changes only if the microsphere diameter exceeded about 50 μm. Although the exact microsphere size needed for receptor stimulation may depend on the experimental conditions, these results strongly suggest that debris moving inside a SCC (canalolithiasis) can produce transcupular pressures able to stimulate ampullar receptors only if they have suitable size, whereas isolated otoconia cannot, except when lying on the cupula (cupulolithiasis).


Author(s):  
Kathleen Boyne ◽  
Deborah A. Corey ◽  
Pan Zhao ◽  
Binyu Lu ◽  
Walter F Boron ◽  
...  

Several aspects of the cell biology of cystic fibrosis (CF) epithelial cells are altered including impaired lipid regulation, disrupted intracellular transport, and impaired microtubule regulation. It is unclear how the loss of cystic fibrosis transmembrane conductance regulator (CFTR) function leads to these differences. It is hypothesized that the loss of CFTR function leads to altered regulation of carbonic anhydrase (CA) activity resulting in cellular phenotypic changes. In this study, it is demonstrated that CA2 protein expression is reduced in CF model cells, primary mouse nasal epithelial (MNE) cells, excised MNE tissue, and primary human nasal epithelial cells (p<0.05). This corresponds to a decrease in CA2 RNA expression measured by qPCR as well as an overall reduction in CA activity in primary CF MNEs. The addition of CFTR-inhibitor-172 to WT MNE cells for ≥24 h mimics the significantly lower protein expression of CA2 in CF cells. Treatment of CF cells with L-Phenylalanine (L-Phe), an activator of CA activity, restores endosomal transport through an effect on microtubule regulation in a manner dependent on soluble adenylate cyclase (sAC). This effect can be blocked with the CA2-selective inhibitor dorzolamide. These data suggest the loss of CFTR function leads to the decreased expression of CA2 resulting in the downstream cell signaling alterations observed in CF.


Author(s):  
L.S. Cutler

Many studies previously have shown that the B-adrenergic agonist isoproterenol and the a-adrenergic agonist norepinephrine will stimulate secretion by the adult rat submandibular (SMG) and parotid glands. Recent data from several laboratories indicates that adrenergic agonists bind to specific receptors on the secretory cell surface and stimulate membrane associated adenylate cyclase activity which generates cyclic AMP. The production of cyclic AMP apparently initiates a cascade of events which culminates in exocytosis. During recent studies in our laboratory it was observed that the adenylate cyclase activity in plasma membrane fractions derived from the prenatal and early neonatal rat submandibular gland was retractile to stimulation by isoproterenol but was stimulated by norepinephrine. In addition, in vitro secretion studies indicated that these prenatal and neonatal glands would not secrete peroxidase in response to isoproterenol but would secrete in response to norepinephrine. In contrast to these in vitro observations, it has been shown that the injection of isoproterenol into the living newborn rat results in secretion of peroxidase by the SMG (1).


Author(s):  
Judith A. Murphy ◽  
Anthony Paparo ◽  
Richard Sparks

Fingernail clams (Muscu1ium transversum) are dominant bottom-dwelling animals in some waters of the midwest U.S. These organisms are key links in food chains leading from nutrients in water and mud to fish and ducks which are utilized by man. In the mid-1950’s, fingernail clams disappeared from a 100-mile section of the Illinois R., a tributary of the Mississippi R. Some factor(s) in the river and/or sediment currently prevent clams from recolonizing areas where they were formerly abundant. Recently, clams developed shell deformities and died without reproducing. The greatest mortality and highest incidence of shell deformities appeared in test chambers containing the highest proportion of river water to well water. The molluscan shell consists of CaCO3, and the tissue concerned in its secretion is the mantle. The source of the carbonate is probably from metabolic CO2 and the maintenance of ionized Ca concentration in the mantle is controlled by carbonic anhydrase. The Ca is stored in extracellular concentric spherical granules(0.6-5.5μm) which represent a large amount of inertCa in the mantle. The purpose of this investigation was to examine the role of raw river water and well water on shell formation in the fingernail clam.


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