Membrane potential calcium-activated channels

Fig. 8. Effects of cannabinoids on synaptic transmission. Activation ofthe CBq receptor at the presynaptic axon terminal inhibits transmitter release from the synaptic vesicle. Three mechanisms can be involved in presynaptic inhibition X refers to unknown second messengers) inhibition of voltage-dependent calcium channels, activation of potassium channels and direct interference with the vesicle release machinery.TheCBi receptor can be activated by exogenous agonists, but also by the endocannahinoids anandamide (A 4) and 2-arachidonoylglycerol (2-AG i, which are released from the postsynaptic neuron by passive and/or facilitated diffusion. The synthesis of endocannahinoids is triggered by a depolarisation-induced ( / , membrane potential) calcium influx or by activation ofGq/n protein-coupled receptors...

The resting membrane potential of most excitable cells is around —60 to —80 mV. This gradient is maintained by the activity of various ion channels. When the potassium channels of the cell open, potassium efflux occurs and hyperpolari2ation results. This decreases calcium channel openings, which ia turn preveats the influx of calcium iato the cell lea ding to a decrease ia iatraceUular calcium ia the smooth muscles of the vasculature. The vascular smooth muscles thea relax and the systemic blood pressure faUs. 

Several different changes in mitochondria occur during apoptosis. These include a change in membrane potential (usually depolarization), increased production of reactive oxygen species, potassium channel activation, calcium ion uptake, increased membrane permeability and release of cytochrome c and apoptosis inducing factor (AIF) [25]. Increased permeability of the mitochondrial membranes is a pivotal event in apoptosis and appears to result from the formation of pores in the membrane the proteins that form such permeability transition pores (PTP) may include a voltage-dependent anion channel (VDAC), the adenine nucleotide translocator, cyclophilin D, the peripheral benzodiazepine receptor, hexokinase and... 

Fig. 4.1. Cellular model illustrating cell types in vascular wall involved in vasorelaxation induced by SERMs. Putative targets of SERMs are indicated within cyan tags. SERMs directly affect L-type VDCC, BK fil subunit in smooth muscle cells, and ER in endothelial cells. L-type VDCC L-type voltage-dependent calcium channel BK calcium-activated large conductance K+ channel PKG protein kinase G eNOS endothelial nitric oxide synthase GC soluble guanylate cyclase cGMP cyclic GM P V electrochemical membrane potential ER estrogen receptor. See text for further details...

Some of the main types of cellular regulation associated with rhythmic behavior are listed in Table III. Regulation of ion channels gives rise to the periodic variation of the membrane potential in nerve and cardiac cells [27, 28 for a recent review of neural rhythms see, for example, Ref. 29]. Regulation of enzyme activity is associated with metabolic oscillations, such as those that occur in glycolysis in yeast and muscle cells. Calcium oscillations originate... 

In sum, the natural tendency will be for sodium, calcium, and chloride ions to flow into the neuron and for potassium ions to flow out, and in so doing to reduce the membrane potential to zero. In reality, this is not so easy. The plasma membrane of the neuron is not very permeable to these ions. If it were, it would be impossible to sustain concentration gradients across it. The rate of passive diffusion of these ions across this membrane is very slow, though not zero, and different for each ion. So how do ions get across the neuronal plasma membrane rapidly There are two ways gated channels and active transport by pumps. 

SOCs, also known as ICRAC (calcium-release activated channels), have been observed in a wide range of cell types (Parekh and Penner, 1997). The defining property is that depletion of intracellular calcium stores results in increased calcium influx at the plasma membrane. The actual SOC that carries this calcium influx may vary between cells, and cloning studies have identified transient receptor potential channel (TRPC) (Parekh and Penner, 1997, Vandebrouck et al., 2002b) and CRACM1 (Peinelt et al., 2006) as candidate genes. Also, the exact mechanism by which SOCs are activated by store depletion has only been partly elucidated, with a role suggested for a calcium sensor on the endoplasmic reticulum (see Peinelt et al., 2006) and for IP3 (Kiselyov et al., 1998). 

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