Effect of low temperature on glutamate-induced intracellular calcium accumulation and cell death in cultured hippocampal neurons

Arai, Hajime; Uto, Akira; Ogawa, Yasuo; Satô, Kiyoshi

doi:10.1016/0304-3940(93)90363-p

Cited by 29 publications

(16 citation statements)

References 10 publications

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“…Although temperature-dependent neuronal death has been attributed to release of glutamate from synaptic vesicles (Arai et al, 1993), intracel- (Mitani et al, 1991) and production of free radicals (Kil et al, 1996), the present findings suggest that Zn 2 þ translocation from Zn 2 þ -enriched (ZEN) neuronal terminals into postsynaptic neurons is also temperature-dependent. The higher the pre/post-TBI brain temperature, the more vesicular zinc was released at 1 h after TBI, and the more TSQ-positive and eosinophilic neurons were identified 6 h after TBI.…”

Section: Discussionmentioning

confidence: 54%

“…Many processes related to neuronal injury are temperature-dependent, including the release of glutamate from synaptic vesicles (Arai et al, 1993;Zornow, 1995), intracellular accumulation of Ca 2 þ (Mitani et al, 1991), modulation of calcium/calmodulin-dependent protein kinase (Churn et al, 1990) and production of free radicals (Kil et al, 1996). Any or all of those temperature dependencies could contribute to the influence of temperature on neuronal injury after TBI.…”

Section: Introductionmentioning

confidence: 99%

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Neurotoxic Zinc Translocation into Hippocampal Neurons is Inhibited by Hypothermia and is Aggravated by Hyperthermia after Traumatic Brain Injury in Rats

Suh

Frederickson

Danscher

2006

J Cereb Blood Flow Metab

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Hypothermia reduces excitotoxic neuronal damage after seizures, cerebral ischemia and traumatic brain injury (TBI), while hyperthermia exacerbates damage from these insults. Presynaptic release of ionic zinc (Zn 2 þ ), translocation and accumulation of Zn 2 þ ions in postsynaptic neurons are important mechanisms of excitotoxic neuronal injury. We hypothesized that temperature-dependent modulation of excitotoxicity is mediated in part by temperature-dependent changes in the synaptic release and translocation of Zn 2 þ . In the present studies, we used autometallographic (AMG) and fluorescent imaging of N-(6-methoxy-8-quinolyl)-para-toluenesulfonamide (TSQ) staining to quantify the influence of temperature on translocation of Zn 2 þ into hippocampal neurons in adult rats after weight drop-induced TBI. The central finding was that TBI-induced Zn 2 þ translocation is strongly influenced by brain temperature. Vesicular Zn 2 þ release was detected by AMG staining 1 h after TBI. At 301C, hippocampus showed almost no evidence of vesicular Zn 2 þ release from presynaptic terminals; at 36.51C, the hippocampus showed around 20% to 30% presynaptic vesicular Zn 2 þ release; and at 391C vesicular Zn 2 þ release was significantly greater (40% to 60%) than at 36.51C. At 6 h after TBI, intracellular Zn 2 þ accumulation was detected by the TSQ staining method, which showed that Zn 2 þ translocation also paralleled the vesicular Zn 2 þ release. Neuronal injury, assessed by counting eosinophilic neurons, also paralleled the translocation of Zn 2 þ , being minimal at 301C and maximal at 391C. We conclude that pathological Zn 2 þ translocation in brain after TBI is temperature-dependent and that hypothermic neuronal protection might be mediated in part by reduced Zn 2 þ translocation.

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Section: Discussionmentioning

confidence: 54%

Section: Introductionmentioning

confidence: 99%

Neurotoxic Zinc Translocation into Hippocampal Neurons is Inhibited by Hypothermia and is Aggravated by Hyperthermia after Traumatic Brain Injury in Rats

Suh

Frederickson

Danscher

2006

J Cereb Blood Flow Metab

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“…While neurons tolerate low temperatures (at least to 30°C; Arai et al 1993;Lucas et al 1994), irreversible changes of neural cells start at »40°C (Iwagami 1996;Lepock 2003;Lepock et al 1983;Willis et al 2000), only about 3°C above quiet rest baseline. Destructive inXuence increases exponentially with slight increases above that level.…”

Section: Brain Hyperthermia As a Factor Inducing And Potentiating Neumentioning

confidence: 99%

Brain temperature fluctuations during physiological and pathological conditions

Kiyatkin

2007

Eur J Appl Physiol

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This review discusses brain temperature as a physiological parameter, which is determined primarily by neural metabolism, regulated by cerebral blood flow, and affected by various environmental factors and drugs. First, we consider normal fluctuations in brain temperature that are induced by salient environmental stimuli and occur during motivated behavior at stable normothermic conditions. Second, we analyze changes in brain temperature induced by various drugs that affect brain and body metabolism and heat dissipation. Third, we consider how these physiological and drug-induced changes in brain temperature are modulated by environmental conditions that diminish heat dissipation. Our focus is psychomotor stimulant drugs and brain hyperthermia as a factor inducing or potentiating neurotoxicity. Finally, we discuss how brain temperature is regulated, what changes in brain temperature reflect, and how these changes may affect neural functions under normal and pathological conditions. Although most discussed data were obtained in animals and several important aspects of brain temperature regulation in humans remain unknown, our focus is on the relevance of these data for human physiology and pathology.

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“…Indeed, 15 min of exposure to either 100 lM or 1 mM glutamate uniformly induced a marked increase in intracellular calcium, with delayed recovery and massive neuronal death under the conditions of both normothermia and moderate hypothermia at 30°C in cultured hippocampal neurons [23]. Moreover, hypothermia at 34 and 28°C did not affect changes in the cytosolic free calcium concentration induced by NMDA in rat cortical brain slices [24].…”

Section: Discussionmentioning

confidence: 98%

Effect of mild and moderate hypothermia on hypoxic injury in nearly pure neuronal culture

Hisano

Morimoto

2010

J Anesth

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Effect of low temperature on glutamate-induced intracellular calcium accumulation and cell death in cultured hippocampal neurons

Cited by 29 publications

References 10 publications

Neurotoxic Zinc Translocation into Hippocampal Neurons is Inhibited by Hypothermia and is Aggravated by Hyperthermia after Traumatic Brain Injury in Rats

Neurotoxic Zinc Translocation into Hippocampal Neurons is Inhibited by Hypothermia and is Aggravated by Hyperthermia after Traumatic Brain Injury in Rats

Brain temperature fluctuations during physiological and pathological conditions

Effect of mild and moderate hypothermia on hypoxic injury in nearly pure neuronal culture

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