Dynamics of mitochondrial [Ca2+] measured with the low-Ca2+-affinity dye rhod-5N

Fuente, Sergio de la; Fonteríz, Rosalba I.; Montero, Mayte; Alvarez, Javier

doi:10.1016/j.ceca.2011.10.007

Cited by 16 publications

(11 citation statements)

References 22 publications

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“…() and modified by Kadirvel et al . (), Rhod‐5N labelling was performed for the first time in mammalian spermatozoa and was thus required to be adapted from somatic cells (Hayato et al ., ; De la Fuente et al ., ).…”

Section: Methodsmentioning

confidence: 97%

Intracellular calcium movements of boar spermatozoa during ‘in vitro’ capacitation and subsequent acrosome exocytosis follow a multiple-storage place, extracellular calcium-dependent model

et al. 2015

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SUMMARYThis work analysed intracellular calcium stores of boar spermatozoa subjected to 'in vitro' capacitation (IVC) and subsequent progesterone-induced acrosome exocytosis (IVAE). Intracellular calcium was analysed through two calcium markers with different physico-chemical properties, Fluo-3 and Rhod-5N. Indicative parameters of IVC and IVAE were also evaluated. Fluo-3 was located at both the midpiece and the whole head. Rhod-5N was present at the sperm head. This distribution did not change in any of the assayed conditions. Induction of IVC was concomitant with an increase in both head and midpiece Ca 2+ signals. Additionally, while IVC induction was concurrent with a significant (p < 0.05) increase in sperm membrane permeability, no significant changes were observed in O 2 consumption and ATP levels. Incubation of boar spermatozoa in the absence of calcium showed a loss of both Ca 2+ labellings concomitantly with the sperm's inability to achieve IVC. The absence of extracellular calcium also induced a severe decrease in the percentage of spermatozoa exhibiting high mitochondrial membrane potential (hMMP). The IVAE was accompanied by a fast increase in both Ca 2+ signalling in control spermatozoa. These peaks were either not detected or much lessened in the absence of calcium. Remarkably, Fluo-3 marking at the midpiece increased after progesterone addition to sperm cells incubated in a medium without Ca 2+. The simultaneous addition of progesterone with the calcium chelant EGTA inhibited IVAE, and this was accompanied by a significant (p < 0.05) decrease in the intensity of progesterone Ca 2+ -induced peak, O 2 consumption and ATP levels. Our results suggest that boar spermatozoa present different calcium deposits with a dynamic equilibrium among them and with the extracellular environment. Additionally, the modulation role of the intracellular calcium in spermatozoa function seems to rely on its precise localization in boar spermatozoa.

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Section: Methodsmentioning

confidence: 97%

Intracellular calcium movements of boar spermatozoa during ‘in vitro’ capacitation and subsequent acrosome exocytosis follow a multiple-storage place, extracellular calcium-dependent model

et al. 2015

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“…6 Calcium uniporter activity was enhanced using Kaempferol, a compound known to increase mitochondrial and overall cytoplasmic Ca 2 þ levels. [31][32][33][34] Calcium uniporter inhibition with Ru360 treatment diminished the stimulus-evoked neuronal activity, BOLD, and CBF responses whereas enhanced mCU activity with Kaempferol treatment, depending on the dose, augmented most stimulus-evoked measures. Collectively, the results confirm our hypotheses and suggest that mitochondrial Ca 2 þ uptake capacity alters neocortical neuronal activity and hemodynamic responses.…”

Section: Introductionmentioning

confidence: 99%

Mitochondrial Calcium Uptake Capacity Modulates Neocortical Excitability

Sanganahalli

Hermán

Hyder

et al. 2013

J Cereb Blood Flow Metab

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Local calcium (Ca 2 þ ) changes regulate central nervous system metabolism and communication integrated by subcellular processes including mitochondrial Ca 2 þ uptake. Mitochondria take up Ca 2 þ through the calcium uniporter (mCU) aided by cytoplasmic microdomains of high Ca 2 þ . Known only in vitro, the in vivo impact of mCU activity may reveal Ca 2 þ -mediated roles of mitochondria in brain signaling and metabolism. From in vitro studies of mitochondrial Ca 2 þ sequestration and cycling in various cell types of the central nervous system, we evaluated ranges of spontaneous and activity-induced Ca 2 þ distributions in multiple subcellular compartments in vivo. We hypothesized that inhibiting (or enhancing) mCU activity would attenuate (or augment) cortical neuronal activity as well as activity-induced hemodynamic responses in an overall cytoplasmic and mitochondrial Ca 2 þ -dependent manner. Spontaneous and sensory-evoked cortical activities were measured by extracellular electrophysiology complemented with dynamic mapping of blood oxygen level dependence and cerebral blood flow. Calcium uniporter activity was inhibited and enhanced pharmacologically, and its impact on the multimodal measures were analyzed in an integrated manner. Ru360, an mCU inhibitor, reduced all stimulus-evoked responses, whereas Kaempferol, an mCU enhancer, augmented all evoked responses. Collectively, the results confirm aforementioned hypotheses and support the Ca 2 þ uptake-mediated integrative role of in vivo mitochondria on neocortical activity.

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“…It is known for long that mitochondria also affect cytosolic Ca 2+ signals, both by buffering ER‐mediated Ca 2+ increases and by releasing Ca 2+ . At rest, intramitochondrial and cytosolic Ca 2+ concentrations are similar . When the level of Ca 2+ increases in the cytosol, it enters into mitochondria through a complex, multistep mechanism (Figure ).…”

Section: C2+ Handling By Mitochondriamentioning

confidence: 99%

Modeling the intracellular organization of calcium signaling

Dupont

2014

WIREs Mechanisms of Disease

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Calcium (Ca²⁺) is a key signaling ion that plays a fundamental role in many cellular processes in most types of tissues and organisms. The versatility of this signaling pathway is remarkable. Depending on the cell type and the stimulus, intracellular Ca²⁺ increases can last over different periods, as short spikes or more sustained signals. From a spatial point of view, they can be localized or invade the whole cell. Such a richness of behaviors is possible thanks to numerous exchange processes with the external medium or internal Ca²⁺ pools, mainly the endoplasmic or sarcoplasmic reticulum and mitochondria. These fluxes are also highly regulated. In order to get an accurate description of the spatiotemporal organization of Ca²⁺ signaling, it is useful to resort to modeling. Thus, each flux can be described by an appropriate kinetic expression. Ca²⁺ dynamics in a given cell type can then be simulated by a modular approach, consisting of the assembly of computational descriptions of the appropriate fluxes and regulations. Modeling can also be used to get insight into the mechanisms of decoding of the Ca²⁺ signals responsible for cellular responses. Cells can use frequency or amplitude coding, as well as take profit of Ca²⁺ oscillations to increase their sensitivity to small average Ca²⁺ increases.

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Dynamics of mitochondrial [Ca2+] measured with the low-Ca2+-affinity dye rhod-5N

Cited by 16 publications

References 22 publications

Intracellular calcium movements of boar spermatozoa during ‘in vitro’ capacitation and subsequent acrosome exocytosis follow a multiple-storage place, extracellular calcium-dependent model

Intracellular calcium movements of boar spermatozoa during ‘in vitro’ capacitation and subsequent acrosome exocytosis follow a multiple-storage place, extracellular calcium-dependent model

Mitochondrial Calcium Uptake Capacity Modulates Neocortical Excitability

Modeling the intracellular organization of calcium signaling

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