The protective effect of hypothermia on hippocampal slices from guinea pig during deprivation of oxygen and glucose

Tanimoto, Michinori; Okada, Yasuhiro

doi:10.1016/0006-8993(87)90448-3

Cited by 44 publications

(9 citation statements)

References 26 publications

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“…Systemic hypothermia, which inhibits neuronal release of glutamate, prevents or reduces neuronal death after cerebral ischemia (Busto et al, 1987(Busto et al, , 1989Churn et al, 1990;Dietrich et al, 1993;Hu et al, 1995;Kil et al, 1996;Minamisawa et al, 1990a;Rosomoff, 1959;Tanimoto and Okada, 1987), prolonged seizures (Liu et al, 1993;Lundgren et al, 1994) and traumatic brain injury (TBI) (Clifton et al, 1991), especially if initiated before an insult. Conversely, hyperthermia aggravates the neuronal death produced by those conditions (Dietrich, 1992;Dietrich et al, 1996;Lundgren et al, 1994;Minamisawa et al, 1990b).…”

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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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: 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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“…So far only a limited number of studies have examined the effects of temperature on ischaemic neurodegeneration using in vitro preparations. Acute slices have been successfully used to study the functional recovery of synaptic transmission following oxygen and glucose deprivation at different temperatures (Tanimoto and Okada 1987;Taylor and Weber 1993;Greiner et al 1998). Although it is possible to infer effects on cell survival from these experiments they cannot be used to reliably predict long-term neuroprotective effects because the survival times of most slice preparations are limited to a few hours.…”

mentioning

confidence: 99%

Intraischaemic hypothermia reduces free radical production and protects against ischaemic insults in cultured hippocampal slices

McManus

Sadgrove²,

Pringle³

et al. 2004

Journal of Neurochemistry

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Hypothermia has been demonstrated to be an effective neuroprotective strategy in a number of models of ischaemic and excitotoxic neurodegeneration in vitro and in vivo. Reduced glutamate release and free radical production have been postulated as potential mechanisms underlying this effect but no definitive mechanism has yet been reported. In the current study, we have used oxygen-glucose deprivation in organotypic hippocampal slice cultures as an in vitro model of cerebral ischaemia. When assessed by propidium iodide fluorescence, reducing the temperature during oxygen-glucose deprivation to 31-33°C was significantly neuroprotective but this effect was lost if the initiation of hypothermia was delayed until the post-insult recovery period. The neuroprotective effects of hypothermia were associated with a significant decrease in both nitric oxide production, as assessed by 3-amino-4-aminomethyl-2¢,7¢-difluorofluorescein fluorescence, and superoxide formation. Further, hypothermia significantly attenuated NMDA-induced nitric oxide formation in the absence of hypoxia/hypoglycaemia. We conclude that the neuroprotective effects of hypothermia are mediated through a reduction in nitric oxide and superoxide formation and that this effect is likely to be downstream of NMDA receptor activation.

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“…In biochemical terms, one of the first and clearest effects of cerebral anoxia is a rise in lactate production and in tissue acidity (Himwich, 1951;Cohen, 1973;Mutch & Hansen, 1984;Siesj6 & Wieloch, 1985;Tanimoto & Okada, 1987;Schiff & Somjen, 1987). The very early onset of increased lactate formation -which is especially marked in cortex and corresponds to the first appearance of slow waves in the electrocorticogram (as already emphasized by Craig & Beecher, 1943) -suggests that acidosis itself may be responsible for the loss of population spikes during anoxia.…”

Section: Introductionmentioning

confidence: 99%

Acidosis and blockade of orthodromic responses caused by anoxia in rat hippocampal slices at different temperatures.

Krnjević

Walz

1990

The Journal of Physiology

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SUMMARY1. Interstitial pH (pH.) and field responses (to stratum radiatum stimulation) were recorded simultaneously with double-barrelled microelectrodes in the CAI region of hippocampal slices from Sprague-Dawley rats.2. Both the relative acidity and amplitude of field responses increased with depth, reaching a maximum near the centre of the slice. When the temperature was raised from 22 to 37°C, this pH. gradient was > 2 times steeper, but the field responses were much diminished.3. Standard anoxic tests (substituting 95 % N2 + 5 % CO2 for 95 % 02 + 5 % CO2, for 2 min) tended to reduce pH0 and population spikes, but these effects were highly temperature sensitive: at -22°C the blocking rate was only 12 3 + 4 6 % and ApHo -0018+0-0157 units, both per minute; corresponding changes at 34-35°C were 67-6 + 11 9 % and -0O065 + 0-0046 units per minute. Highly significant linear correlations between rates of block and ApHR gave a mean slope of 904 + 17-6 % per 0-1 unit of acid change.4. Anoxia caused similar temperature-dependent increases in acidity in stratum pyramidale and radiatum, but in the latter field responses (EPSPs) were much less depressed after 2 min of anoxia.5. When slices were superfused with acid medium (low [HCO3-j), much greater reductions in pHo were needed to depress responses, giving a mean slope of 17-7 % per 0.1 pH unit.6. In glucose-free medium, there was a slow alkaline shift in pHo (0-13 +0-036 units); population spikes and the acid transients evoked by anoxia disappeared.7. It was concluded that acidosis cannot be the immediate cause of the similar depressions of postsynaptic excitability seen during anoxia and hypoglyeaemia.8. In further tests, DL-p-hydroxyphenyl-lactic acid, a blocker of lactate transport, failed to diminish acid transients evoked by anoxia, indicating that these are not mediated principally by lactate transport.

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The protective effect of hypothermia on hippocampal slices from guinea pig during deprivation of oxygen and glucose

Cited by 44 publications

References 26 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

Intraischaemic hypothermia reduces free radical production and protects against ischaemic insults in cultured hippocampal slices

Acidosis and blockade of orthodromic responses caused by anoxia in rat hippocampal slices at different temperatures.

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