Note that neither the dense pigment granule (G) nor the tear in the section (T) generate mass thickness artifacts in the calcium map. The resolution of the map is high enough to reveal the punctate nature of mitochondrial calcium sequestration e.g. some mitochondria (1, 2 and 3) have taken up little if any calcium, while others (4, 5, 6 and 7) have accumulated much more. The field shown contains seven mitochondria, illustrating the general heterogeneity of mitochondrial calcium accumulation, i.e. Right panel: quantitative EFTEM map of the mitochondrial calcium distribution, recorded as described previously. Left panel: zero-loss structural EFTEM image of an ultra-thin cryosection prepared from a rapidly frozen frog sympathetic neuron 5 min after termination of a 2 min depolarization with 50 mM K +. Calcium ions entering injured cells will activate phospholipases, disrupt mitochondrial electron transport, and release free radicals. Depolarization in the distal regions of the apical dendrite affects the neuron’s firing behavior differently than somatic depolarization by evoking calcium action potentials (Ca 2+ -APs) and bursts of somatic APs ( 3, 4 ). No claim to original US government works.Įnergy-filtered TEM (EFTEM) map of mitochondrial calcium distribution in a depolarization activated frog sympathetic neuron. Calcium ions initiate and regulate responses of central nervous tissues to injury. Non-NMDA receptor mechanisms of excitotoxicity are discussed briefly. The presence of Ca-activated (SK) potassium channels in the spine head provides a negative-feedback loop regulating synaptic depolarization. Finally, we consider the relationship between delayed calcium de-regulation, the mitochondrial permeability transition and the generation of reactive oxygen species, and propose a unified view of the 'source specificity' and 'calcium overload' models of N-methyl-d-aspartate (NMDA) receptor-dependent excitotoxicity. Topics addressed include methodologies for measuring local intracellular calcium, mitochondrial calcium buffering and loading capacity, mitochondrially directed spatial calcium gradients, and the role of calcium overload-dependent mitochondrial dysfunction in glutamate-evoked excitotoxic injury and neurodegeneration. In this review, we consider the basic chemistry of calcium as a 'sticky' cation, which leads to extremely high bound/free ratios, and discuss areas of current interest or controversy. In neurons, mitochondria can accumulate enormous amounts of calcium, with the consequence that mitochondrial calcium uptake, sequestration and release play pivotal roles in orchestrating calcium-dependent responses as diverse as gene transcription and cell death. Calcium is an extraordinarily versatile signaling ion, encoding cellular responses to a wide variety of external stimuli.
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