Membrane permeability to calcium

The depolarization that accompanies the action potential induces an increase in membrane permeability to calcium ions. A large inward electrochemical gradient exists for calcium and it moves into the terminal. The calcium that enters the terminal activates enzymes that cause the attachment of some of the vesicles to releasing sites on the terminal membrane, membrane fusion, and the release of the vesicular contents into the synaptic cleft. Transmitter release is terminated by the removal of calcium from the terminal cytoplasm, either via a calcium pump, which pumps it out of the cell, or by uptake into the endoplasmic reticulum or into mitochondria. 

These findings provided evidence that the mechanism by which epinephrine stimulates platelet functional change is through enhanced membrane permeability to calcium. This effect of epinephrine appears to be in marked contrast to the mechanism of ADP-stimulation which is presumably mediated through internal Ca2+ release. 

Mechanism Praziquantel increases membrane permeability to calcium, causing marked contraction initially and then paralysis of tiematode muscles this is followed by vacuolization and parasite death. 

Intracellular ionized calcium acts as a second messenger, coupling the action of a hormone or electrical impulse (the first messenger) on the outside of the cell to intracellular events, such as hormone or protein secretion, protein kinase activity, or muscle contraction. The effect of Ca on intracellular processes is often mediated by a small calcium-binding protein, such as troponin C in muscle (Chapter 21) or calmodulin in many other cells (Chapters 15 and 30). Synthesis of these calciumbinding proteins is not directly affected by vitamin D or any of its metabolites. Many stimuli that affect permeability to calcium also activate membrane-bound adenylate cyclase and increase the intracellular concentration of cAMP (Chapter 30). 

Intracellular calcium is kept very low by all organisms. An increase in the intracellular calcium content is used in intracellular signalling and prolonged increases can trigger stress reactions. Thus it was believed that viscosinamide could make the membrane more permeable to calcium. 

Inhibition of Calcium Movement. Figure 15 shows that cromoglycate inhibits membrane permeability to 45-calclum over the same concentration range for the inhibition of histamine release. Furthermore when cromoglycate was compared with dibutyryl cyclic AMP and doxantrazole, the relative potencies of the drugs for inhibition of histamine release (doxantrazole cromoglycate dibutyryl... 

Hormones secreted in the hypothalamus, which releases pituitary hormones, are believed to bind to specific receptors of the membranes of the pituicyte. This action is dependent upon the presence of Ca Therefore, it has been proposed that the hormone depolarizes the cell membrane increasing the permeability to calcium which would, in turn, release the hormone. Whatever the role of calcium, it is known in the case of thyroid releasing hormone that it stimulates adenylcyclase and cAMP. 

Since it is known that the ionophore X-537A increases the membrane permeability to divalent cations we incubated toad retinas in Ames-Hastings medium during 20 minutes in darkness in the presence of different calcium concentrations here again the uptake is Ca " -dependent. When 27 yg/ml (40 yM) of ionophore was added, the incorporation in total lipids increased and the higher labeling was found in PA and PI. 

Other studies, in agreement with our data, have shown that PVC-membranes are permeable to calcium ions and linear Mackay plots are obtained, which indicate that a liquid ion-exchanger process is taking place. The CBS membrane containing only sensor (no mediator) is impermeable to Ca " " and gave a curved Mackay plot which is behaviour typical of a solid ion-exchanger. When a mediator is present (DOPP) the behaviour becomes more like a liquid ion-exchanger system. 

Calciunvchannel binding increases the membrane s permeability to calcium and enhances depolarization. 

Amyloid pore An oligomer of amyloid proteins that forms a channel, generally permeable to calcium ions, in the plasma membrane of brain cells in patients with neurodegenerative diseases. Pore oligomers are considered as the more toxic forms of amyloid proteins. 

It has been found that the axon membrane may have negatively charged sites at its surface [1]. The variation of the membrane permeability to cations in the presence of calcium ions has been related to their adsorption on these sites [2] the chemical nature of which is ignored yet. 

Mitochondrial permeability transition involves the opening of a larger channel in the inner mitochondrial membrane leading to free radical generation, release of calcium into the cytosol and caspase activation. These alterations in mitochondrial permeability lead eventually to disruption of the respiratory chain and dqDletion of ATP. This in turn leads to release of soluble intramito-chondrial membrane proteins such as cytochrome C and apoptosis-inducing factor, which results in apoptosis. 

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