Plasma membranes calcium channels

Plasma membrane channels. The most common mechanism for the movement of into smooth muscle cells Ifom the extracellular space is the electrodiffusion of Ca " ions through highly selective channels. This movement can be significant in two quite different ways. First, Ca ions carry two positive charges and, in fact, most of the inward charge movement across the plasma membrane of smooth muscle myocytes is carried by Ca. Most smooth muscle action potentials are known to be Ca " action potentials. And second, the concentration of intracellular free calcium, the second messenger, is increased by inward calcium movement. 

In those secretory tissues where extracellular calcium is necessary for secretion, calcium enters by way of plasma membrane channels. Therefore, the nature of membrane channels is obviously very important. Are the channels uniform on a given cell Do their characteristics vary from tissue to tissue Many questions remain unanswered, but several studies suggest that a cell may have more than one type of calcium channel. Although not a secretory tissue, smooth muscle has two types of calcium channel potential sensitive channels and receptor operated channels (30). So, in this tissue [and probably in secretory tissues as well (31)], the nature of the stimulus may determine which channels are opened, the extent of calcium entry and the extent of the response. A high potassium solution, which is commonly used to activate calcium mediated responses, would open potential dependent channels whereas drugs acting on their respective receptors would open a different set of channels, but cause the same overall response. 

It is noteworthy that the inactivation of the Heliothis RyR at millimolar [Ca ] was prevented at all flubendiamide concentrations tested. This could plausibly explain the insecticidal mechanism since deactivation of calcium release channels at high [Ca ] would be essential to terminate the intracellular calcium transient (27). According to this hypothesis, ryanodine receptors would be fixed in the (sub)conductance conformation leading to calcium store depletion and, possibly, to subsequent activation of capacitative calcium entry through plasma membrane channels. This would override compensatory calcium removal mechanisms such as the sarcoplasmic Ca-ATPase (SERCA) activity and the sodium-calcium exchanger (NCX) in the plasma membrmie. The sustained high intracellular [Ca would finally lead to muscle contraction paralysis that is consistently observed in flubendiamide-affected lepidopteran larvae. 

In addition to intracellular heme-containing proteins, big-conductance calcium-dependent K+ (BKCa) channels and calcium-spark activated transient Kca channels in plasma membrane are also tar geted by CO [3]. As well known, nitric oxide (NO) also activates BKca channels in vascular smooth muscle cells. While both NO and CO open BKCa channels, CO mainly acts on alpha subunit of BKCa channels and NO mainly acts on beta subunit of BKca channels in vascular smooth muscle cells. Rather than a redundant machinery, CO and NO provide a coordinated regulation of BKca channel function by acting on different subunits of the same protein complex. Furthermore, pretreatment of vascular smooth muscle... 

Calcium channels in the plasma membrane activated after receptor-mediated calcium release from intracellular stores. Diese channels are present in many cellular types and play pivotal roles in a multitude of cell functions. It was recently shown that Orai proteins are the pore-forming subunit of CRAC channels. They are activated by STIM proteins that sense the Ca2+ content of the endoplasmic reticulum. 

The NHR contains also the conserved Calcineurin docking site, PxlxIT, required for the physical interaction of NEAT and Calcineurin. Dephosphorylation of at least 13 serines residues in the NHR induces a conformational change that exposes the nuclear localization sequences (NLS), allowing the nuclear translocation of NEAT. Rephosphorylation of these residues unmasks the nuclear export sequences that direct transport back to the cytoplasm. Engagement of receptors such as the antigen receptors in T and B cells is coupled to phospholipase C activation and subsequent production of inositol triphosphate. Increased levels of inositol triphosphate lead to the initial release of intracellular stores of calcium. This early increase of calcium induces opening of the plasma membrane calcium-released-activated-calcium (CRAC) channels,... 

Calcium channels are members of the large family of proteins, including Na and channels, which become incorporated into plasma membranes, and which form intermittent aqueous pathways through which ions can move. The channels open and close. As is the case generally for membrane spanning proteins, a Ca channel is formed by a set of helical units, in this case seven, which associate to form the channel. 

Sarcoplasmic reticulum Ca -channels. In many smooth muscle cells the rise of intracellular calcium which triggers contraction comes from the flow of calcium from the SR through Ca channels. In others, the SR contributes some unknown fraction of the triggering calcium relative to the amount which comes from the extracellular space through the plasma membrane Ca -channels. There are at least two kinds of Ca -channels in the SR. 

Ca2+ can enter cells via voltage- or ligand-dependent channels and by capacitative entry. These three fundamental mechanisms of regulated calcium ion entry across the plasma membrane involve, respectively, voltage-dependent Ca2+ channels, ligand-gated Ca2+ channels and capacitative Ca2+ entry associated with phospholipase C-coupled receptors. 

In regards to necrosis, it is clear that the old adage an ounce of prevention is worth a pound of cure applies. Agents that stabilize ion homeostasis have proved to be effective in preventing necrosis in cell culture studies. For example, drugs that activate plasma membrane potassium ion channels or chloride ion channels can prevent membrane depolarization and so inhibit sodium and calcium ion influx. Agents that prevent large sustained increases in intracellular free calcium levels can also prevent neuronal... 

The molecules that transduce noxious heat or cold are members of the transient receptor potential (TRP) receptor family. TRP proteins (Table 57-2) form tetra-meric nonselective cation channels within the plasma membrane, allowing sodium and calcium ion influx [4]. The TRPV3 channel is activated at temperatures between 31 and39°C, TRPV1 at43°C, and TRPV2 at 52-55°C. The heat pain threshold in humans is 43°C, suggesting that... 

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