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Cholera toxin:

This toxin binds to GM1 gangliosides on the outer membrane surface of the intestinal mucosa cells. The toxin activates the cell's adenylate cyclase enzyme to become continually active.

The increased adenylate cyclase results in an abnormally high amount of cyclic AMP (cAMP), which in turn causes the cells to excrete large amounts of Cl- into the intestines. Electrolytes, including Na+, and water follow the osmotic and electric gradients created by the excretion of Cl-. It is this "pumping" of water and electrolytes that cause the diarrhea and dehydration seen in the disease.


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Discussion Starter · #3 ·
thanx , so the toxin has no role in production of new receptors ,but just attacks the original receptors , or does high level of cAMP can induce receptor synthesis ?
 

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thanx , so the toxin has no role in production of new receptors ,but just attacks the original receptors , or does high level of cAMP can induce receptor synthesis ?
Affects the receptors that are there, they in turn will produce the products that lead to the diarrhea (as said above secretion of electrolytes into the lumen along with water)
 

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As patelmd and aktorque said... cAMP activates PKA which phosphorylates the CFTR channel. The pattern is the familiar; the target in this case is the CFTR chloride channel, just like with heat-labile enterotoxin.
 
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