The Ca2+-induced membrane transition in mitochondria

Rhodamine 123 staining and electron microscopy were used to reveal a correlation between the ultrastructural and functional state of cultured cerebellar granule cells after short glutamate treatment. Glutamate exposure (15 min, 100 lxM) in Mg2+-free solution caused considerable ultrastructural alterations in a granule cell: clumping of the chromatin, swelling of the endoplasmic reticulum and mitochondria, and disruption of the mitochondrial cristae. After glutamate treatment, the mitochondria of the neurons lost their ability to sequester rhodamine 123. Both the N-methyl-D-nspartate receptor channel blocker MK-801 (30 ItM) and cobalt chloride (2 mM) prevented the deteriorative effects of glutamate. These data suggest that glutaumte-induced Ca 2+ overload of the neurons can lead to nonspecific permeability of the inner mitochondrial membrane, resulting in neuronal death.

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Section: Resultsmentioning

confidence: 99%

Neurotoxic glutamate treatment of cultured cerebellar granule cells induces Ca²⁺‐dependent collapse of mitochondrial membrane potential and ultrastructural alterations of mitochondria

et al. 1996

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“…Reagents that stabilize the "c"-conformation such as carboxyatractyloside, sensitize mPT to Ca 2+ while reagents that stabilize the "m"-conformation such as ADP and bongkrekic acid, made mPT less sensitive to Ca 2+ [56][57][58][59]. Direct evidence for the presence of ANT in the PTP complex came from work of Woodfield et al [60] that used a Cyp D affinity column to identify proteins that are part of the PTP.…”

Section: Adp/atp Translocase (Ant)mentioning

confidence: 99%

Mitochondrial carriers and pores: Key regulators of the mitochondrial apoptotic program?

2007

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Mitochondria play a pivotal role in the process of apoptosis. Alterations in mitochondrial structure and function during apoptosis are regulated by proteins of the BCL-2 family, however their exact mechanism of action is largely unknown. Mitochondrial carriers and pores play an essential role in maintaining the normal function of mitochondria, and BCL-2 family members were shown to interact with several mitochondrial carriers/pores and to affect their function. This review focuses on the involvement of several of these mitochondrial carriers/pores in the regulation of the mitochondrial death pathway.

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“…The mitochondrial permeability transition has been characterized by the pioneering work of Hunter and Haworth and corresponds to the sudden increase in the permeability of the inner mitochondrial membrane to molecules of molecular mass up to 1,500 Da (Haworth & Hunter, 1979; Hunter & Haworth, 1979a, 1979b). The opening is due to a nonspecific pore called the mitochondrial permeability transition pore (mPTP) occurring when mitochondria become overloaded with calcium.…”

Section: Introductionmentioning

confidence: 99%

Mitochondria and aging: A role for the mitochondrial transition pore?

2018

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SummaryThe cellular mechanisms responsible for aging are poorly understood. Aging is considered as a degenerative process induced by the accumulation of cellular lesions leading progressively to organ dysfunction and death. The free radical theory of aging has long been considered the most relevant to explain the mechanisms of aging. As the mitochondrion is an important source of reactive oxygen species (ROS), this organelle is regarded as a key intracellular player in this process and a large amount of data supports the role of mitochondrial ROS production during aging. Thus, mitochondrial ROS, oxidative damage, aging, and aging‐dependent diseases are strongly connected. However, other features of mitochondrial physiology and dysfunction have been recently implicated in the development of the aging process. Here, we examine the potential role of the mitochondrial permeability transition pore (mPTP) in normal aging and in aging‐associated diseases.

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The Ca2+-induced membrane transition in mitochondria

Cited by 677 publications

References 19 publications

Neurotoxic glutamate treatment of cultured cerebellar granule cells induces Ca²⁺‐dependent collapse of mitochondrial membrane potential and ultrastructural alterations of mitochondria

Neurotoxic glutamate treatment of cultured cerebellar granule cells induces Ca²⁺‐dependent collapse of mitochondrial membrane potential and ultrastructural alterations of mitochondria

Mitochondrial carriers and pores: Key regulators of the mitochondrial apoptotic program?

Mitochondria and aging: A role for the mitochondrial transition pore?

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The Ca2+-induced membrane transition in mitochondria

Cited by 677 publications

References 19 publications

Neurotoxic glutamate treatment of cultured cerebellar granule cells induces Ca2+‐dependent collapse of mitochondrial membrane potential and ultrastructural alterations of mitochondria

Neurotoxic glutamate treatment of cultured cerebellar granule cells induces Ca2+‐dependent collapse of mitochondrial membrane potential and ultrastructural alterations of mitochondria

Mitochondrial carriers and pores: Key regulators of the mitochondrial apoptotic program?

Mitochondria and aging: A role for the mitochondrial transition pore?

Contact Info

Product

Resources

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Neurotoxic glutamate treatment of cultured cerebellar granule cells induces Ca²⁺‐dependent collapse of mitochondrial membrane potential and ultrastructural alterations of mitochondria

Neurotoxic glutamate treatment of cultured cerebellar granule cells induces Ca²⁺‐dependent collapse of mitochondrial membrane potential and ultrastructural alterations of mitochondria