Calcium-dependent glutamate release concomitant with massive potassium flux during cerebral ischemia in vivo

Katayama, Yoichi; Kawamata, Tatsuro; Tamura, Toru; Hovda, David A.; Becker, Donald P.; Takata, Takashi

doi:10.1016/0006-8993(91)90730-j

Cited by 164 publications

(62 citation statements)

References 22 publications

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“…2D1-D3). Thus, there are at least two possible sources of Glu efflux: one is the Ca 2+ -dependent release from glutaminergic nerve endings (Drejer et al, 1985;Katayama et al, 1991), and the other is the reversed operation of neuronal and/or astrocytic Glu reuptake transporters (Phillis et al, 2000;Roettger and Lipton, 1996;Szatkowski et al, 1990).…”

Section: Resultsmentioning

confidence: 99%

Reversed operation of glutamate transporter GLT‐1 is crucial to the development of preconditioning‐induced ischemic tolerance of neurons in neuron/astrocyte co‐cultures

Kikuchi

Kosugi

Tanaka

et al. 2004

Glia

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Sublethal ischemia leads to increased tolerance against subsequent prolonged cerebral ischemia in vivo. In the present study, we investigated the roles of the astrocytic glutamate (Glu) transporter GLT-1 in preconditioning (PC)-induced neuronal ischemic tolerance in cortical neuron/astrocyte co-cultures. Ischemia in vitro was simulated by subjecting cultures to both oxygen and glucose deprivation (OGD). A sublethal OGD (PC) significantly increased the survival rate of neurons when cultures were exposed to a lethal OGD 24 hr later. The extracellular concentration of Glu increased significantly during PC, and treatment with an inhibitor of NMDA receptors significantly reversed the PC-induced ischemic tolerance of neurons, suggesting that the increase in extracellular concentration of Glu during PC was critical to the development of PC-induced neuronal ischemic tolerance via the activation of NMDA receptors. Treatment with a GLT-1 blocker during PC significantly suppressed this increase in Glu, and antagonized the PC-induced neuronal ischemic tolerance. This study suggested that the reversed operation of GLT-1 was crucial to the development of neuronal ischemic tolerance.2

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Section: Resultsmentioning

confidence: 99%

Reversed operation of glutamate transporter GLT‐1 is crucial to the development of preconditioning‐induced ischemic tolerance of neurons in neuron/astrocyte co‐cultures

Kikuchi

Kosugi

Tanaka

et al. 2004

Glia

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“…Evidence for both vesicular (Drejer et al 1985;Hershkowitz et al 1993) and non-vesicular (Szatkowski et al 1990;Pocock and Nicholls 1998) glutamate release during ischemia have been provided. It appears that in the early phase of ischemia, glutamate is released by a Ca 2+ -dependent vesicular mechanism (Katayama et al 1991;Wahl et al 1994;Pocock and Nicholls 1998;Asai et al 2000), which is followed by a Ca 2+ -independent non-vesicular release (Sanchez-Prieto and Gonzalez 1988; Ikeda et al 1989;Szatkowski et al 1990;Kawakami et al 2001). Real time glutamate measurement in an in vitro model of ischemia showed that glutamate uptake is inhibited within a few minutes of the onset of ischemia (Jabaudou et al 2000).…”

Section: Discussionmentioning

confidence: 99%

Glutamate release by an Na⁺ load and oxidative stress in nerve terminals: relevance to ischemia/reperfusion

Tretter

Ádám-Vizi

2002

Journal of Neurochemistry

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“…It is known that the excitotoxic hypothesis of ischemic neuronal death is based on neurotoxic effects of high extracellular concentrations of glutamate release as the result of enhanced excitatory synaptic activity (Katayama et al, 1991;Limbrick et al, 2003). This toxicity is largely related to calcium influx into affected nerve cells (Kristian & Siesjö, 1998).…”

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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Calcium-dependent glutamate release concomitant with massive potassium flux during cerebral ischemia in vivo

Cited by 164 publications

References 22 publications

Reversed operation of glutamate transporter GLT‐1 is crucial to the development of preconditioning‐induced ischemic tolerance of neurons in neuron/astrocyte co‐cultures

Reversed operation of glutamate transporter GLT‐1 is crucial to the development of preconditioning‐induced ischemic tolerance of neurons in neuron/astrocyte co‐cultures

Glutamate release by an Na⁺ load and oxidative stress in nerve terminals: relevance to ischemia/reperfusion

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

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Calcium-dependent glutamate release concomitant with massive potassium flux during cerebral ischemia in vivo

Cited by 164 publications

References 22 publications

Reversed operation of glutamate transporter GLT‐1 is crucial to the development of preconditioning‐induced ischemic tolerance of neurons in neuron/astrocyte co‐cultures

Reversed operation of glutamate transporter GLT‐1 is crucial to the development of preconditioning‐induced ischemic tolerance of neurons in neuron/astrocyte co‐cultures

Glutamate release by an Na+ load and oxidative stress in nerve terminals: relevance to ischemia/reperfusion

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

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Glutamate release by an Na⁺ load and oxidative stress in nerve terminals: relevance to ischemia/reperfusion