Minor trauma prevents hippocampal delayed neuronal death after transient ischemia
نویسندگان
چکیده
منابع مشابه
Selective dysfunction of hippocampal CA1 astrocytes contributes to delayed neuronal damage after transient forebrain ischemia.
Transient global ischemia, as with cardiac arrest, causes loss of CA1 hippocampal neurons 2-4 d later, whereas nearby dentate gyrus (DG) neurons are relatively resistant. Whether differential astrocyte vulnerability in ischemic injury contributes to CA1 neuronal death is uncertain. Here, we find that CA1 astrocytes are more sensitive to ischemia than DG astrocytes. In rats subjected to transien...
متن کاملThe PIDDosome mediates delayed death of hippocampal CA1 neurons after transient global cerebral ischemia in rats.
A brief period of global brain ischemia, such as that induced by cardiac arrest or cardiopulmonary bypass surgery, causes cell death in vulnerable hippocampal CA1 pyramidal neurons days after reperfusion. Although numerous factors have been suggested to account for this phenomenon, the mechanisms underlying it are poorly understood. We describe a cell death signal called the PIDDosome, a protei...
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BACKGROUND AND PURPOSE p53-upregulated modulator of apoptosis (PUMA), a BH3-only member of the Bcl-2 protein family, is required for p53-dependent and -independent forms of apoptosis. PUMA localizes to mitochondria and interacts with antiapoptotic Bcl-2 and Bcl-X(L) or proapoptotic Bax in response to death stimuli. Although studies have shown that PUMA is associated with pathomechanisms of cere...
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Transient cerebral ischemia (TCI) occurs when blood flow to the brain is ceased or dramatically reduced. TCI causes energy depletion and oxidative stress, which leads to neuronal death and cognitive impairment. Dichloroacetic acid (DCA) acts as an inhibitor of pyruvate dehydrogenase kinase (PDK). Additionally, DCA is known to increase mitochondrial pyruvate uptake and promotes glucose oxidation...
متن کاملPhagocytosis executes delayed neuronal death after focal brain ischemia.
Delayed neuronal loss and brain atrophy after cerebral ischemia contribute to stroke and dementia pathology, but the mechanisms are poorly understood. Phagocytic removal of neurons is generally assumed to be beneficial and to occur only after neuronal death. However, we report herein that inhibition of phagocytosis can prevent delayed loss and death of functional neurons after transient brain i...
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ژورنال
عنوان ژورنال: Japanese Journal of Pharmacology
سال: 1989
ISSN: 0021-5198
DOI: 10.1016/s0021-5198(19)56635-5