Neuroscience

Edited by: Steve Bunk M. Ankarcrona, J.M. Dypbukt, E. Bonfoco, B. Zhivotovsky, S. Orrenius, S.A. Lipton, P. Nicotera, "Glutamate-induced neuronal death: A succession of necrosis or apoptosis depending on mitochondrial function," Neuron, 15:961-73, 1995. (Cited in 120 papers through October 1997) Comments by Stuart A. Lipton, Cerebrovascular and NeuroScience Research Institute, Brigham and Women's Hospital and Program in Neuroscience, Harvard Medical School; and Pierluigi Nicotera, Molecular To

The Scientist Staff
Nov 23, 1997

Edited by: Steve Bunk
M. Ankarcrona, J.M. Dypbukt, E. Bonfoco, B. Zhivotovsky, S. Orrenius, S.A. Lipton, P. Nicotera, "Glutamate-induced neuronal death: A succession of necrosis or apoptosis depending on mitochondrial function," Neuron, 15:961-73, 1995. (Cited in 120 papers through October 1997)

Comments by Stuart A. Lipton, Cerebrovascular and NeuroScience Research Institute, Brigham and Women's Hospital and Program in Neuroscience, Harvard Medical School; and Pierluigi Nicotera, Molecular Toxicology Program, University of Konstanz, Germany

When a region of an injured brain is deprived of blood and oxygen, there are two ways the cells can die, by necrosis or by apoptosis. The mode of death makes a big difference to surrounding tissue. In the study that prompted this paper, a multinational team discovered that the functioning of a brain neuron's mitochondria-the energy-producing organelles outside the nucleus-is the critical determinant of how the cell dies during blood-deprived or ischemic brain injury, as...

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