• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

大鼠海马锥体层中刺激诱发的细胞外钾离子和钙离子变化。

Stimulation-evoked changes in extracellular K+ and Ca2+ in pyramidal layers of the rat's hippocampus.

作者信息

Krnjević K, Morris M E, Reiffenstein R J

出版信息

Can J Physiol Pharmacol. 1982 Dec;60(12):1643-57. doi: 10.1139/y82-243.

DOI:10.1139/y82-243
PMID:7165860
Abstract

In urethane-anaesthetized rats, ion-selective microelectrodes recorded changes in extracellular K+ and Ca2+ concentrations (delta[K+]omicron and delta[Ca2+]omicron) in pyramidal layers of the hippocampus (mostly in area CA1), which were evoked by fimbrial-commissural stimulation. [K+]omicron increased linearly with frequency of stimulation up to a critical frequency, in the range of 2-5 Hz, where bursts of population spikes appeared, and then rose rapidly to reach a ceiling of 9-12 mM. During continued stimulation, [K+]omicron remained well above the resting level of about 3.0 mM. At the end of stimulation [K+]omicron returned to the base line with a half time of 4-8 s, and a minor undershoot of congruent to 0.5 mM was detectable for 1-2 min. When stimulating at frequencies above the critical value, a sharp fall in [Ca2+]omicron (by an average of one-third below the mean resting level of 1.4 mM) consistently started 1-5 s after the onset of the rapid phase of delta[K+]omicron. [Ca2+]omicron typically reached a minimum in 5-10 s and immediately started to return towards the base line. The recovery of [Ca2+]omicron was often accelerated by an overshoot of up to 0.3 mM; this was followed by a delayed phase of low [Ca2+]omicron for another 2-3 min. During prolonged stimulation at frequencies near 7 Hz, both [Ca2+]omicron and [K+]omicron fluctuated periodically, in time with the appearance and disappearance of bursts of population spikes. Comparable observations were made in area CA2-3 (just external to CA1); in the deeper areas of CA3, in CA4, and in the dentate gyrus, major changes in [K+]omicron and [Ca2+]omicron (as well as bursts of population spikes) were evoked only by prolonged fimbrial stimulation at higher frequencies (congruent to 10 Hz). Thus, although adequate repetitive stimulation of fimbrial-commissural inputs evokes sharp but opposite changes in [K+]omicron and [Ca2+]omicron, the fall in [Ca2+]omicron is consistently much briefer than the rise in [K+]omicron, presumably because of the evanescent character of postsynaptic Ca2+ spikes.

摘要

在氨基甲酸乙酯麻醉的大鼠中,离子选择性微电极记录了海马锥体细胞层(主要在CA1区)细胞外K⁺和Ca²⁺浓度的变化(Δ[K⁺]₀和Δ[Ca²⁺]₀),这些变化由穹窿 - 连合刺激诱发。[K⁺]₀随刺激频率线性增加,直至达到临界频率(2 - 5Hz范围),此时出现群体峰电位爆发,然后迅速上升至9 - 12mM的上限。在持续刺激期间,[K⁺]₀保持在远高于约3.0mM的静息水平之上。刺激结束时,[K⁺]₀以4 - 8秒的半衰期回到基线,并且在1 - 2分钟内可检测到约0.5mM的轻微下冲。当以高于临界值的频率刺激时,[Ca²⁺]₀在Δ[K⁺]₀快速上升阶段开始后1 - 5秒持续急剧下降(平均比1.4mM的平均静息水平低三分之一)。[Ca²⁺]₀通常在5 - 10秒内达到最小值并立即开始向基线恢复。[Ca²⁺]₀的恢复常因高达0.3mM的上冲而加速;随后是低[Ca²⁺]₀的延迟阶段,持续另外2 - 3分钟。在接近7Hz的频率下长时间刺激期间,[Ca²⁺]₀和[K⁺]₀都随群体峰电位爆发的出现和消失而周期性波动。在CA2 - 3区(CA1区外侧)也有类似观察结果;在CA3更深区域、CA4和齿状回中,只有通过更高频率(约10Hz)的长时间穹窿刺激才能诱发[K⁺]₀和[Ca²⁺]₀的主要变化(以及群体峰电位爆发)。因此,尽管对穹窿 - 连合输入进行充分的重复刺激会诱发[K⁺]₀和[Ca²⁺]₀急剧但相反的变化,但[Ca²⁺]₀的下降始终比[K⁺]₀的上升短暂得多,这可能是由于突触后Ca²⁺峰电位的短暂特性。

相似文献

1
Stimulation-evoked changes in extracellular K+ and Ca2+ in pyramidal layers of the rat's hippocampus.大鼠海马锥体层中刺激诱发的细胞外钾离子和钙离子变化。
Can J Physiol Pharmacol. 1982 Dec;60(12):1643-57. doi: 10.1139/y82-243.
2
Depth distribution and mechanism of changes in extracellular K+ and Ca2+ concentrations in the hippocampus.海马体中细胞外钾离子和钙离子浓度的深度分布及变化机制。
Can J Physiol Pharmacol. 1982 Dec;60(12):1658-71. doi: 10.1139/y82-244.
3
Induction of paroxysmal discharges in the dentate gyrus: frequency dependence and relationship to afterdischarge production.齿状回中阵发性放电的诱导:频率依赖性及其与后放电产生的关系。
J Neurophysiol. 1989 Jul;62(1):126-35. doi: 10.1152/jn.1989.62.1.126.
4
Prolonged field bursts in the dentate gyrus: dependence on low calcium, high potassium, and nonsynaptic mechanisms.齿状回中的长时程场爆发:对低钙、高钾和非突触机制的依赖性。
J Neurophysiol. 1992 Dec;68(6):2016-25. doi: 10.1152/jn.1992.68.6.2016.
5
Changes in extracellular Ca2+ and K+ activity accompanying hippocampal discharges.海马放电时细胞外钙离子和钾离子活性的变化。
Can J Physiol Pharmacol. 1980 May;58(5):579-82. doi: 10.1139/y80-097.
6
Aspartate and glutamate induced reductions in extracellular free calcium and sodium concentration in area CA1 of 'in vitro' hippocampal slices of rats.天冬氨酸和谷氨酸可使大鼠“体外”海马脑片CA1区细胞外游离钙和钠浓度降低。
Neurosci Lett. 1983 Jan 31;35(1):79-84. doi: 10.1016/0304-3940(83)90530-x.
7
Nonsynaptic epileptogenesis in the mammalian hippocampus in vitro. II. Role of extracellular potassium.体外培养的哺乳动物海马中的非突触性癫痫发生。II. 细胞外钾的作用。
J Neurophysiol. 1986 Aug;56(2):424-38. doi: 10.1152/jn.1986.56.2.424.
8
Activity-evoked increases in extracellular potassium modulate presynaptic excitability in the CA1 region of the hippocampus.活动诱发的细胞外钾离子增加调节海马体CA1区的突触前兴奋性。
J Neurophysiol. 1987 Aug;58(2):404-16. doi: 10.1152/jn.1987.58.2.404.
9
Analysis of potential shifts associated with recurrent spreading depression and prolonged unstable spreading depression induced by microdialysis of elevated K+ in hippocampus of anesthetized rats.对麻醉大鼠海马体中通过微量透析升高钾离子诱导的反复性扩散性抑制和持续性不稳定扩散性抑制相关潜在变化的分析。
Brain Res. 1993 May 7;610(2):283-94. doi: 10.1016/0006-8993(93)91412-l.
10
Effects of changes in extracellular potassium, magnesium and calcium concentration on synaptic transmission in area CA1 and the dentate gyrus of rat hippocampal slices.细胞外钾、镁和钙浓度变化对大鼠海马脑片CA1区和齿状回突触传递的影响。
Pflugers Arch. 1990 Feb;415(5):588-93. doi: 10.1007/BF02583510.

引用本文的文献

1
Interstitial ions: A key regulator of state-dependent neural activity?间质离子:状态依赖型神经活动的关键调节因子?
Prog Neurobiol. 2020 Oct;193:101802. doi: 10.1016/j.pneurobio.2020.101802. Epub 2020 May 13.
2
Calcium homeostasis modulator 1 (CALHM1) is the pore-forming subunit of an ion channel that mediates extracellular Ca2+ regulation of neuronal excitability.钙稳态调节蛋白 1(CALHM1)是一种离子通道的形成孔亚基,介导细胞外 Ca2+ 对神经元兴奋性的调节。
Proc Natl Acad Sci U S A. 2012 Jul 10;109(28):E1963-71. doi: 10.1073/pnas.1204023109. Epub 2012 Jun 18.
3
Hippocampal betaine/GABA transporter mRNA expression is not regulated by inflammation or dehydration post-status epilepticus.
海马甜菜碱/GABA 转运体 mRNA 表达不受癫痫后炎症或脱水的调节。
J Neurochem. 2011 Apr;117(1):82-90. doi: 10.1111/j.1471-4159.2011.07174.x. Epub 2011 Feb 9.
4
Repetitive perforant-path stimulation induces epileptiform bursts in minislices of dentate gyrus from rats with kainate-induced epilepsy.反复穿通纤维刺激在红藻氨酸诱导癫痫大鼠的齿状回小切片中诱导癫痫样爆发。
J Neurophysiol. 2011 Feb;105(2):522-7. doi: 10.1152/jn.00456.2010. Epub 2010 Dec 8.
5
Implication of Kir4.1 channel in excess potassium clearance: an in vivo study on anesthetized glial-conditional Kir4.1 knock-out mice.Kir4.1 通道在钾离子清除过多中的作用:麻醉条件性 Kir4.1 敲除小鼠的体内研究。
J Neurosci. 2010 Nov 24;30(47):15769-77. doi: 10.1523/JNEUROSCI.2078-10.2010.
6
Calcium-induced conformational transition of trout ependymins monitored by tryptophan fluorescence.通过色氨酸荧光监测的钙诱导的鳟鱼室管膜蛋白构象转变。
Open Biochem J. 2009;3:14-7. doi: 10.2174/1874091X00903010014. Epub 2009 Feb 24.
7
Computer simulations of neuron-glia interactions mediated by ion flux.由离子通量介导的神经元-神经胶质细胞相互作用的计算机模拟。
J Comput Neurosci. 2008 Oct;25(2):349-65. doi: 10.1007/s10827-008-0083-9. Epub 2008 Feb 23.
8
Regulation of extracellular calcium in the hippocampus in vivo during epileptiform activity--role of astrocytes.癫痫样活动期间体内海马体中细胞外钙的调节——星形胶质细胞的作用。
Epilepsy Res. 2007 May;74(2-3):155-62. doi: 10.1016/j.eplepsyres.2007.03.005. Epub 2007 Apr 16.
9
N-cadherin signaling in synapse formation and neuronal physiology.N-钙黏蛋白信号在突触形成和神经元生理学中的作用
Mol Neurobiol. 2006 Jun;33(3):237-52. doi: 10.1385/MN:33:3:237.
10
Kv7/KCNQ/M-channels in rat glutamatergic hippocampal axons and their role in regulation of excitability and transmitter release.大鼠谷氨酸能海马轴突中的Kv7/KCNQ/M通道及其在兴奋性调节和递质释放中的作用。
J Physiol. 2006 Oct 1;576(Pt 1):235-56. doi: 10.1113/jphysiol.2006.111336. Epub 2006 Jul 13.