Cerebral hypoxia-ischemia in immature rats: Involvement of mitochondrial permeability transition?

Developmental Neuroscience

Volumn 23, Issue 3, 2001, Pages 192-197

  Puka Sundvall, Malgorzata ^a   Gilland, Eric ^a   Hagberg, Henrik ^a  

^a UNIVERSITY OF GOTHENBURG   (Sweden)

Author keywords

Brain damage; Hypoxia ischemia; Immature rats; Mitochondria; Neonatal rats; Permeability transition

Indexed keywords

CYCLOSPORIN A; DEOXYGLUCOSE;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; BRAIN CORTEX; BRAIN HYPOXIA; BRAIN INJURY; BRAIN ISCHEMIA; BRAIN MITOCHONDRION; BRAIN PERFUSION; CELL MEMBRANE PERMEABILITY; CONFERENCE PAPER; CONTROLLED STUDY; DISEASE COURSE; DRUG EFFECT; MITOCHONDRIAL RESPIRATION; NEUROPROTECTION; NEWBORN; NONHUMAN; PRIORITY JOURNAL; RAT;

ANIMALS; ANIMALS, NEWBORN; BRAIN; CARBON RADIOISOTOPES; CYCLOSPORINE; ENZYME INHIBITORS; GLUCOSE-6-PHOSPHATE; HYPOXIA-ISCHEMIA, BRAIN; MITOCHONDRIA; RATS;

EID: 0035742481     PISSN: 03785866     EISSN: None     Source Type: Journal    
DOI: 10.1159/000046142     Document Type: Conference Paper

References (46)

1. Mitochondrial control of apoptosis
2. Cyclosporin A, but not FK 506, protects mitochondria and neurons against hypoglycemic damage and implicates the mitochondrial permeability transition in cell death
3. Mitochondria in neurodegeneration: Acute ischemia and chronic neurodegenerative diseases
4. Mitochondrial function and energy metabolism after hypoxia-ischemia in the immature rat brain: Involvement of NMDA-receptors
5. Mitochondrial function after asphyxia in newborn lambs
6. Impairment of mitochondrial respiration after cerebral hypoxia-ischemia in immature rats: Relationship to activation of caspase-3 and neuronal injury
7. Subcellular distribution of calcium and ultrastructural changes after hypoxia-ischemia in immature rats
8. The mitochondrial permeability transition pore and its role in cell death
9. The mitochondrial death/life regulator in apoptosis and necrosis
10. The mitochondrial permeability transition: From biochemical curiosity to pathophysiological mechanism
11. Blockade of the mitochondrial permeability transition pore diminishes infarct size in the rat after transient middle cerebral artery occlusion
12. Amelioration by cyclosporin A of brain damage in transient forebrain ischemia in the rat
13. The influence of immaturity on hypoxic-ischemic brain damage in the rat
14. Pathogenesis of hypoxic-ischemic brain injury in a perinatal rodent model
15. Neuropathology of remote hypoxic-ischemic damage in the immature rat
16. Mitochondrial non-specific pores remain closed during cardiac ischaemia, but open upon reperfusion
17. Elucidating the molecular mechanism of the permeability transition pore and its role in reperfusion injury of the heart
18. NMDA receptor-dependent increase of cerebral glucose utilization after hypoxia-ischemia in the immature rat
19. Citrate synthase
20. Protein measurement with the folin phenol reagent
21. Evaluation of brain damage in a rat model of neonatal hypoxic-ischemia
22. Expression of classical mitochondrial respiratory responses in homogenates of rat forebrain
23. 14C]deoxyglucose method for the measurement of the local cerebral glucose utilization: Theory, procedure, and normal values in the conscious and anesthetized albino rat
24. Formation of free radicals in hypoxic-ischemic brain damage in the neonatal rat, assessed by an endogenous spin trap and lipid peroxidation
25. Free radicals are formed in the brain of fetal sheep during reperfusion after cerebral ischemia
26. Carbohydrate and energy metabolism during the evolution of hypoxic-ischemic brain damage in the immature rat
27. Cerebral energy metabolism during hypoxia-ischemia and early recovery in immature rats
28. Cerebral oxidative metabolism and redox state during hypoxia-ischemia and early recovery in immature rats
29. Alterations in glutathione and amino acid concentrations after hypoxia-ischemia in the immature rat brain
30. Calcium accumulation during the evolution of hypoxic-ischemic brain damage in the immature rat
31. Cyclosporin A protects against ischemia-reperfusion injury in the brain
32. Permeability of the blood-brain barrier to the immunosuppressive cyclic peptide cyclosporin A
33. Restrictive transport of a lipid-soluble peptide (cyclosporin) through the blood-brain barrier
34. In vivo evidence for ATP-dependent and P-glycoprotein-mediated transport of cyclosporin A at the blood-brain barrier
35. Physiologic modeling of cyclosporin kinetics in rat and man
36. 2+-induced large-amplitude swelling of liver and heart mitochondria by cyclosporin is probably caused by the inhibitor binding to mitochondrial-matrix peptidyl-prolyl cis-trans isomerase and preventing it interacting with the adenine nucleotide translocase
37. Further evidence that cyclosporin A protects mitochondria from calcium overload by inhibiting a matrix peptidyl-prolyl cis-trans isomerase. Implications for the immunosuppressive and toxic effects of cyclosporin
38. The development of the human blood-CSF-brain barrier
39. The development of the human blood-brain and blood-CSF barriers
40. Vulnerability to cerebral hypoxic-ischemic insult in neonatal but not in adult rats is in parallel with disruption of the blood-brain barrier
41. Cyclosporin A binding to mitochondrial cyclophilin inhibits the permeability transition pore and protects hearts from ischaemia/reperfusion injury
42. Recruitment of mitochondrial cyclophilin to the mitochondrial inner membrane under conditions of oxidative stress that enhance the opening of a calcium-sensitive non-specific channel
43. The permeability transition in heart mitochondria is regulated synergistically by ADP and cyclosporin A
44. Magnesium ion modulates the sensitivity of the mitochondrial permeability transition pore to cyclosporin A and ADP
45. Mitochondrial dysfunction in neurodegenerative diseases
46. Neuronal excitotoxicity: The role of mitochondria