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Ecological evidence indicates a worldwide trend of dramatically decreased soil Ca2+ levels caused by increased acid deposition andmassive timber harvesting. Little is known about the genetic and cellularmechanismof plants' responses to Ca2+ depletion. In this study, transcriptional profiling analysis helped identify multiple extracellular Ca2+ ([Ca2+]ext) depletion-responsive genes in Arabidopsis thaliana L.,many ofwhich are involved in response to other environmental stresses. Interestingly, a group of genes encoding putative cytosolic Ca2+ ([Ca2+]cyt) sensors were significantly upregulated, implying that [Ca2+]cyt has a role in sensing [Ca2+]ext depletion. Consistent with this observation, [Ca2+]ext depletion stimulated a transient rise in [Ca2+]cyt that was negatively influenced by [K+]ext, suggesting the involvement of amembrane potential-sensitive component. The [Ca2+]cyt response to [Ca2+]ext depletion was significantly desensitized after the initial treatment, which is typical of a receptor-mediated signaling event. The response was insensitive to an animal Ca2+ sensor antagonist, but was suppressed by neomycin, an inhibitor of phospholipase C. Gd3+, an inhibitor of Ca2+ channels, suppressed the [Ca2+]ext-triggered rise in [Ca2+]cyt and downstream changes in gene expression. Taken together, this study demonstrates that [Ca2+]cyt plays an important role in the putative receptor-mediated cellular and transcriptional response to [Ca2+]ext depletion of plant cells. [ABSTRACT FROM AUTHOR]

Ecological evidence indicates a worldwide trend of dramatically decreased soil Ca2+ levels caused by increased acid deposition andmassive timber harvesting. Little is known about the genetic and cellularmechanismof plants' responses to Ca2+ depletion. In this study, transcriptional profiling analysis helped identify multiple extracellular Ca2+ ([Ca2+]ext) depletion-responsive genes in Arabidopsis thaliana L.,many ofwhich are involved in response to other environmental stresses. Interestingly, a group of genes encoding putative cytosolic Ca2+ ([Ca2+]cyt) sensors were significantly upregulated, implying that [Ca2+]cyt has a role in sensing [Ca2+]ext depletion. Consistent with this observation, [Ca2+]ext depletion stimulated a transient rise in [Ca2+]cyt that was negatively influenced by [K+]ext, suggesting the involvement of amembrane potential-sensitive component. The [Ca2+]cyt response to [Ca2+]ext depletion was significantly desensitized after the initial treatment, which is typical of a receptor-mediated signaling event. The response was insensitive to an animal Ca2+ sensor antagonist, but was suppressed by neomycin, an inhibitor of phospholipase C. Gd3+, an inhibitor of Ca2+ channels, suppressed the [Ca2+]ext-triggered rise in [Ca2+]cyt and downstream changes in gene expression. Taken together, this study demonstrates that [Ca2+]cyt plays an important role in the putative receptor-mediated cellular and transcriptional response to [Ca2+]ext depletion of plant cells. [ABSTRACT FROM AUTHOR]

Aim: Cardiac basal metabolism upon extracellular calcium removal and its relationship with intracellular sodium and calcium homeostasis was evaluated. Methods: A mechano-calorimetric technique was used that allowed the simultaneous and continuous measurement of both heat rate and resting pressure in arterially perfused quiescent adult rat hearts. Using pharmacological tools, the possible underlying mechanisms related to sodium and calcium movements were investigated. Results: Resting heat rate (expressed in mW g−1dry wt) increased upon calcium withdrawal (+4.4 ± 0.2). This response was: (1) unaffected by the presence of tetrodotoxin (+4.3 ± 0.6), (2) fully blocked by both, the decrease in extracellular sodium concentration and the increase in extracellular magnesium concentration, (3) partially blocked by the presence of either nifedipine (+2.8 ± 0.4), KB-R7943 (KBR; +2.5 ± 0.2), clonazepam (CLO; +3.1 ± 0.3) or EGTA (+1.9 ± 0.3). The steady heat rate under Ca2+-free conditions was partially reduced by the addition of Ru360 (−1.1 ± 0.2) but not CLO in the presence of EGTA, KBR or Ru360. Conclusion: Energy expenditure for resting state maintenance upon calcium withdrawal depends on the intracellular rise in both sodium and calcium. Our data are consistent with a mitochondrial Ca2+ cycling, not detectable under normal calcium diastolic levels. The experimental condition here analysed, partially simulates findings reported under certain pathological situations including heart failure in which mildly increased levels of both diastolic sodium and calcium have also been found. Therefore, under such pathological conditions, hearts should distract chemical energy to fuel processes associated with sodium and calcium handling, making more expensive the maintenance of their functions. [ABSTRACT FROM AUTHOR]

Voltage-gated Ca2+ channels activated by action potentials evoke Ca2+ entry into presynaptic terminals thus briefly distorting the resting Ca2+ concentration. When this happens, a number of processes are initiated to re-establish the Ca2+ equilibrium. During the post-spike period, the increased Ca2+ concentration could enhance the presynaptic Ca2+ signalling. Some of the mechanisms contributing to presynaptic Ca2+ dynamics involve endogenous Ca2+ buffers, Ca2+ stores, mitochondria, the sodium–calcium exchanger, extraterminal Ca2+ depletion and presynaptic receptors. Additionally, subthreshold presynaptic depolarization has been proposed to have an effect on release of neurotransmitters through a mechanism involving changes in resting Ca2+. Direct evidence for the role of any of these participants in shaping the presynaptic Ca2+ dynamics comes from direct recordings of giant presynaptic terminals and from fluorescent Ca2+ imaging of axonal boutons. Here, some of this evidence is presented and discussed. [ABSTRACT FROM AUTHOR]