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Long-term potentiation of glutamatergic transmission and epileptiform activity induced by transient episodes of anoxia in slices of rats hippocampus field CA1.

作者信息

Kalemenev S V, Savin A V, Levin S G, Godukhin O V

机构信息

Institute of Theoretical and Experimental Biophysics, Russian Academy of Sciences, Pushchino, Moscow Region.

出版信息

Neurosci Behav Physiol. 2002 Jul-Aug;32(4):431-4. doi: 10.1023/a:1015840529841.

DOI:10.1023/a:1015840529841
PMID:12243265
Abstract
摘要

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1
Long-term potentiation of glutamatergic transmission and epileptiform activity induced by transient episodes of anoxia in slices of rats hippocampus field CA1.大鼠海马CA1区切片中短暂性缺氧发作所诱导的谷氨酸能传递的长期增强和癫痫样活动。
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2
[Long-term potentiation of glutamatergic transmission and epileptiform activity induced by short-term episodes of anoxia in the CA1 field of the rat hippocampal slices].[大鼠海马切片CA1区短期缺氧发作诱导的谷氨酸能传递长期增强和癫痫样活动]
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Increasing age reduces expression of long-term depression and dynamic range of transmission plasticity in CA1 field of the rat hippocampus.年龄增长会降低大鼠海马体CA1区的长时程抑制表达以及传递可塑性的动态范围。
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Increases in the threshold for the development of epileptiform activity in field CA1 of Krushinskii-Molodnika rat hippocampal slices as an adaptive protective mechanism.作为一种适应性保护机制，克鲁申斯基-莫洛德尼卡大鼠海马切片CA1区癫痫样活动发展阈值的升高。
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Rapid plasticity at inhibitory and excitatory synapses in the hippocampus induced by ictal epileptiform discharges.发作期癫痫样放电诱导海马中抑制性和兴奋性突触的快速可塑性。
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Nitric oxide signalling is required for the generation of anoxia-induced long-term potentiation in the hippocampus.一氧化氮信号传导是海马体中缺氧诱导的长时程增强产生所必需的。
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The role of long-term potentiation in persistent epileptiform burst-induced hyperexcitability following GABAA receptor blockade.γ-氨基丁酸A受体阻断后，长时程增强在持续性癫痫样爆发诱导的兴奋性增强中的作用。
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Characterization of the anoxia-induced long-term synaptic potentiation in area CA1 of the rat hippocampus.大鼠海马体CA1区缺氧诱导的长期突触增强的特征
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本文引用的文献

1
Acute and chronic increases in excitability in rat hippocampal slices after perinatal hypoxia In vivo.围产期缺氧后大鼠海马切片体内兴奋性的急性和慢性增加
J Neurophysiol. 1998 Jan;79(1):73-81. doi: 10.1152/jn.1998.79.1.73.
2
The effects of neonatal hypoxia on kindled seizure development and electroconvulsive shock profiles.
Epilepsia. 1996 Aug;37(8):723-7. doi: 10.1111/j.1528-1157.1996.tb00642.x.
3
Evidence disputing the link between seizure activity and high extracellular glutamate.质疑癫痫发作活动与细胞外谷氨酸水平升高之间联系的证据。
J Neurochem. 1996 Jun;66(6):2446-54. doi: 10.1046/j.1471-4159.1996.66062446.x.
4
Hypoxic-ischemic encephalopathy sustained in early postnatal life may result in permanent epileptic activity and an altered cortical convulsive threshold in rat.出生后早期持续存在的缺氧缺血性脑病可能导致大鼠永久性癫痫活动和皮质惊厥阈值改变。
Epilepsy Res. 1994 Jan;17(1):31-42. doi: 10.1016/0920-1211(94)90077-9.
5
Anoxic LTP sheds light on the multiple facets of NMDA receptors.
Trends Neurosci. 1994 Nov;17(11):497-503. doi: 10.1016/0166-2236(94)90140-6.
6
Long-term effect of postnatal hypoxia on the seizure susceptibility in rats.产后缺氧对大鼠癫痫易感性的长期影响。
Life Sci. 1985 Oct 28;37(17):1597-604. doi: 10.1016/0024-3205(85)90478-3.