Discussion of all aspects of cellular structure, physiology and communication.
4 posts • Page 1 of 1
Ok, so i have been studying various processes of animal physiology in a little detail and have noticed something that arose a question, one which i haven't been able to answer, regardless of how much searching i did.
The neuron stores some vesicles with neurotransmitter in the tip of the axon, which only fuse with the plasma membrane to release the neurotransmitter by exocytosis when an action potential arrives. This is done by the opening of voltage mediated calcium channels, which cause an influx of calcium at that point. The calcium inactivates the protein synaptotogmin, which allows the SNARE complex to form and fusion of the vesicle with the membrane to take place.
BUT some other processes seem to have a calicum-mediated exocytosis mechanism. Among these, fusion of cortical granules with the plasma membrane in the fertilised egg, fusion of vesicles with the GLUT4 transporter with the membrane induced by insulin and fusion of the vesicle with aquaporins in them stimulated by ADH.
The question is:
Are all these processes mediated by proteins of the synaptotogmin family? Or are mediated by another mechanism, perhaps maybe calmodulin? Although i don't see how, since calmodulin is part of a protein kinase right?
i'm not sure if i'm answering the question your asking but i just thought i'd point out that the initial depolarisation responsible for calcium mediated exocytosis can occur in diffferent ways...
1) Opening of sodium channels - e.g. which as you said occurs in presynpatic neurones and results in neurotransmitter release
2) Closure of potassium channels... e.g. in the beta cells of the pancreas....
- glucose enters -> glycolysis occurs -> ATP generated -> ATP causes closure of potassium channels -> depolarisation -> calcium influx -> release of vesicles containing insulin -> insulin causes upregulation of Glut 4 transporters thus causing increased uptake of glucose into cells
I think you are asking too hard a question for me to answer... I don't know what secondary messangers are involved in each process... but i just thought i'd make the point about the depolarisation...
yes, the action potential is generated in different ways, but why should that count? Generally points in the pathway are responsible for protein-ligand interactions, which need to be the same in common pathways. A depolarization in the membrane is the same thingn regardless of what caused it, and voltage-dependent channels open regardless of what caused the membrane potential to shift
Because it's absolutely vital for designing drugs and knowing how they work...
e.g. sodium channel blockers are used treating grand mal epilepsy, for treating cardiac dysrhymias, for local anasthesia..etc.
potassium channel blockers are widely used to treat type II diabetics (causes more insulin release) among other things...
so tis an important difference...
4 posts • Page 1 of 1
Who is online
Users browsing this forum: No registered users and 1 guest