Reduced calcium elevation in hippocampal CA1 neurons of ischemia-tolerant gerbils

Shimazaki, Kuniko; Nakamura, Takeshi; Nakamura, Kyoko; Oguro, Keiji; Masuzawa, Toshio; Kudo, Yoshihisa; Kawai, Nobufumi

doi:10.1097/00001756-199806010-00038

Cited by 42 publications

(29 citation statements)

References 7 publications

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“…When ischemic preconditioning preceded a lethal 5 min of forebrain ischemia in gerbils, several potentially beneficial changes were found in hippocampal CA1 neurons, including the following: plasma membrane Ca 2ϩ -ATPase activities were elevated before the test ischemia, and remained subsequently at a higher level, and mitochondrial sequestration Ca 2ϩ was enhanced (285). In line with these data, imaging of intracellular Ca 2ϩ ([Ca 2ϩ ] i ) showed that its elevation in hippocampal CA1 neurons after an anoxic-aglycemic episode was markedly inhibited in the ischemia-tolerant gerbil (367). Furthermore, also in the hippocampus of gerbils, the expression of the plasma membrane Ca 2ϩ -ATPase isoform 1 (PMCA1) was increased, together with that of inducible 72-kDa heat shock protein (HSP70), when brain ischemic tolerance was enhanced by 3-nitropropionic acid preconditioning (190).…”

Section: Cellular Ionic Homeostasis In the Ischemiatolerant Brainmentioning

confidence: 65%

Molecular Physiology of Preconditioning-Induced Brain Tolerance to Ischemia

Obrenovitch¹

2008

Physiological Reviews

228

176

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Ischemic tolerance describes the adaptive biological response of cells and organs that is initiated by preconditioning (i.e., exposure to stressor of mild severity) and the associated period during which their resistance to ischemia is markedly increased. This topic is attracting much attention because preconditioning-induced ischemic tolerance is an effective experimental probe to understand how the brain protects itself. This review is focused on the molecular and related functional changes that are associated with, and may contribute to, brain ischemic tolerance. When the tolerant brain is subjected to ischemia, the resulting insult severity (i.e., residual blood flow, disruption of cellular transmembrane gradients) appears to be the same as in the naive brain, but the ensuing lesion is substantially reduced. This suggests that the adaptive changes in the tolerant brain may be primarily directed against postischemic and delayed processes that contribute to ischemic damage, but adaptive changes that are beneficial during the subsequent test insult cannot be ruled out. It has become clear that multiple effectors contribute to ischemic tolerance, including: 1) activation of fundamental cellular defense mechanisms such as antioxidant systems, heat shock proteins, and cell death/survival determinants; 2) responses at tissue level, especially reduced inflammatory responsiveness; and 3) a shift of the neuronal excitatory/inhibitory balance toward inhibition. Accordingly, an improved knowledge of preconditioning/ischemic tolerance should help us to identify neuroprotective strategies that are similar in nature to combination therapy, hence potentially capable of suppressing the multiple, parallel pathophysiological events that cause ischemic brain damage.

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Section: Cellular Ionic Homeostasis In the Ischemiatolerant Brainmentioning

confidence: 65%

Molecular Physiology of Preconditioning-Induced Brain Tolerance to Ischemia

Obrenovitch¹

2008

Physiological Reviews

228

176

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“…In the early stage after ischemic insult, Bcl-2 was shown to protect against the excitotoxicity of glutamate, 23 and to regulate the movement of Ca 2+ through the membranes of the endoplasmic reticulum and mitochondoria, thus eliminating the Ca 2+ signal for cell death. 24,25 We have shown that intracellular Ca 2+ elevation in CA1 neurons after ischemia was markedly inhibited in ischemia-tolerant gerbils, 26 in the same period when Bcl-2 was elevated in CA1 area. 11 These data suggest the protective action of Bcl-2 in the early stage of delayed neuronal death.…”

Section: Discussionmentioning

confidence: 95%

Adeno-associated virus vector-mediated bcl-2 gene transfer into post-ischemic gerbil brain in vivo: prospects for gene therapy of ischemia-induced neuronal death

et al. 2000

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The proto-oncogene bcl-2 is known as an anti-apoptotic gene that confers the ability to block neuronal cell death after transient ischemia. In order to examine whether the bcl-2 gene can be used for protection of ischemic brain injury, we generated adeno-associated virus (AAV) vectors capable of expressing human bcl-2. Replication-defective AAV vectors were found effectively to transfer and express bcl-2 gene in the gerbil hippocampal neurons. Transduction with AAV bcl-2 5 days before forebrain ischemia prevented the DNA frag-

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“…Shimazaki et al (1998) reported that the intracellular calcium influx in ischemia-tolerant neurons is markedly inhibited after an anoxic-aglycemic episode, as compared with neurons in control animals, and Lin et al (2008) showed that preconditioning with glutamate confers neuroprotection against subsequent oxygen-glucose deprivation in cultured cortical neurons. Furthermore, our results showed that glutamate release in multiple 5 min ischemic episodes was reduced subsequently by induced cerebral ischemic tolerance which inhibited intracellular calcium influx.…”

Section: Discussionmentioning

confidence: 99%

The Effect of Extracellular Glutamate Release on Repetitive Transient Ischemic Injury in Global Ischemia Model

Lee

Choi

et al. 2009

Korean J Physiol Pharmacol

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During operations, neurosurgeons usually perform multiple temporary occlusions of parental artery, possibly resulting in the neuronal damage. It is generally thought that neuronal damage by cerebral ischemia is associated with extracellular concentrations of the excitatory amino acids. In this study, we measured the dynamics of extracellular glutamate release in 11 vessel occlusion (VO) model to compare between single occlusion and repeated transient occlusions within short interval. Changes in cerebral blood flow were monitored by laser-Doppler flowmetry simultaneously with cortical glutamate level measured by amperometric biosensor. From real time monitoring of glutamate release in 11 VO model, the change of extracellular glutamate level in repeated transient occlusion group was smaller than that of single occlusion group, and the onset time of glutamate release in the second ischemic episode of repeated occlusion group was delayed compared to the first ischemic episode which was similar to that of single 10 min ischemic episode. These results suggested that repeated transient occlusion induces less glutamate release from neuronal cell than single occlusion, and the delayed onset time of glutamate release is attributed to endogeneous protective mechanism of ischemic tolerance.

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Reduced calcium elevation in hippocampal CA1 neurons of ischemia-tolerant gerbils

Cited by 42 publications

References 7 publications

Molecular Physiology of Preconditioning-Induced Brain Tolerance to Ischemia

Molecular Physiology of Preconditioning-Induced Brain Tolerance to Ischemia

Adeno-associated virus vector-mediated bcl-2 gene transfer into post-ischemic gerbil brain in vivo: prospects for gene therapy of ischemia-induced neuronal death

The Effect of Extracellular Glutamate Release on Repetitive Transient Ischemic Injury in Global Ischemia Model

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