Calcium transients and intramembrane charge movement in skeletal muscle fibres

Myoplasmic calcium transients in response to pulse depolarisations have been monitored using the dye antipyralazo III, which provides a linear measure of the change in cytoplasmic free calcium concentration. Intramembrane charge movements were recorded simultaneously with the calcium transients. Except for its initial phase, the calcium transient during each pulse closely followed the time course expected for calcium redistribution between three intracellular compartments with time-independent flux coefficients. The time at which the flux coefficients attained their steady values occurred just after the intramembrane charge movement had been completed. This is the required sequence if charge movement were to control one or more coefficients f or calcium fluxes across the sarcoplasmic reliculum membrane.     

Calcium transients in astrocyte endfeet cause cerebrovascular constrictions

Cerebral blood flow (CBF) is coupled to neuronal activity and is imaged in vivo to map brain activation. CBF is also modified by afferent projection fibres that release vasoactive neurotransmitters in the perivascular region, principally on the astrocyte endfeet that outline cerebral blood vessels. However, the role of astrocytes in the regulation of cerebrovascular tone remains uncertain. Here we determine the impact of intracellular Ca(2+) concentrations ([Ca(2+)](i)) in astrocytes on the diameter of small arterioles by using two-photon Ca(2+) uncaging to increase [Ca(2+)](i). Vascular constrictions occurred when Ca(2+) waves evoked by uncaging propagated into the astrocyte endfeet and caused large increases in [Ca(2+)](i). The vasoactive neurotransmitter noradrenaline increased [Ca(2+)](i) in the astrocyte endfeet, the peak of which preceded the onset of arteriole constriction. Depressing increases in astrocyte [Ca(2+)](i) with BAPTA inhibited the vascular constrictions in noradrenaline. We find that constrictions induced in the cerebrovasculature by increased [Ca(2+)](i) in astrocyte endfeet are generated through the phospholipase A(2)-arachidonic acid pathway and 20-hydroxyeicosatetraenoic acid production. Vasoconstriction by astrocytes is a previously unknown mechanism for the regulation of CBF.