Ca2 + -activated K + channel

This subfamily including the large- (BKCa), intermediate-(IKca), and small-conductance (SKCa) Ca2+-activated K + channels are activated by increases in intracellular free Ca2+ concentration. The opening of DCca and SKCa channels are less voltage-dependent, whereas the activation of BKCa channel has steep voltage sensitivity. 

From the earliest measurements of tissue calcium, it was clear that total calcium is largely a measure of stored calcium. Through the years, scientists have used a variety of indirect measures of [Ca2+]j. These include shortening of or tension in muscles secretion from secretory cells the activity of Ca2+-dependent enzymes, most notably glycogen phosphorylase and flux of K+, or K+ currents, as a reflection of Ca2+-activated K+ channels. In addition, investigators often use the radioactive calcium ion [45Ca2+] as an indirect indicator of Ca2+ concentrations and Ca2+ movements. 

STOCs arise from the concerted activation of up to 100 Ca2+-activated K+ channels (KCa) in the sarcolemma as a consequence of Ca2+ release from the SR. This release may take the form either of non-propagating focal events such as sparks or puffs , or of more regenerative Ca2+ waves. Since a temporal correlation between them exists, STOCs have been attributed to focal nonpropagating Ca2+ release events. However, this view requires that each STOC is a spatially restricted membrane current that occurs at selected areas of membrane closely apposed to the SR. While essential to the prevalent hypothesis for STOCs,... 

Young We have data showing that induction of a Ca2+ wave in cultured myometrial cells that lack L-type Ca2+ channels causes activation of Ca2+-activated K+ channels that we think are store-operated. This is just with passage of a Ca2+ wave without thapsigargin. 

Transient spontaneous increases in intracellular ionized Ca2+ concentration, [Ca2+] , were first detected in smooth muscle as bursts of openings of Ca2+ activated K+ channels (Benham Bolton 1986). Several years later, laser scanning confocal imaging showed that similar spontaneous transient increases in... 

During the action potential in vas deferens or urinary bladder the rise in [Ca2+] close under the cell membrane is responsible, in combination with the depolarization, for the repolarization phase as it causes the opening of Ca2+-activated K+ channels through which a large repolarizing outward current flows (Arnaudeau et al 1997, Imaizumi et al 1998, Ohi et al 2001). This may lead to a transient period of hyperpolarization (an afterhyperpolarization ) following the action potential (Imaizumi et al 1998). 

ZhuGe R, Fogarty KE, Tuft RA, Lifshitz LM, Sayar K, Walsh JV 2000 Dynamics of signaling between Ca2+ sparks and Ca2+-activated K+ channels studied with a novel image-based method for direct intracellular measurement of ryanodine receptor Ca2+ current. J Gen... 

Cox DH, Aid rich RW 2000 Role of the /) 1 subunit in large-conductance Ca2+-activated K+ channel gating energetics mechanisms of enhanced Ca2+ sensitivity. J Gen Physiol 116 411-432... 

Petkov GV, Bonev AD, Heppner TJ, Brenner R, Aldrich RW, Nelson MT 2001 / l-subunit of the Ca2+-activated K+ channel regulates contractile activity of mouse urinary bladder smooth muscle. J Physiol 537 443-452... 

Rousseau E, Smith JS, Meissner G 1987 Ryanodine modifies conductance and gating behavior of single Ca2+ release channel. Am J Physiol 253 C364—C368 Wallner M, Meera P, Toro L 1999 Molecular basis of fast inactivation in voltage and Ca2+-activated K+ channels a transmembrane /) subunit homolog. Proc Natl Acad Sci USA 96 4137-4142... 

Wellman GC, Santana LF, Bonev AD, Nelson MT 2001 Role of phospholamban in the modulation of arterial Ca2+ sparks and Ca2+-activated K+ channels by cAMP. Am J Physiol 281 C1029-0037... 

The i.c.v. injection of apamin or charybdotoxin, specific blockers of the SK and BK type of Ca2+-activated K+ channels, respectively, prevented the antinociception mediated by tricyclic antidepressants and H1 histamine receptor antagonists whereas 0C2 adrenoceptor-mediated supraspinal analgesia did not depend on the activation of these K+ channels (Table 1). 

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