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4-氨基吡啶诱导幼年大鼠海马同步活动期间的细胞外游离钾

Extracellular free potassium during synchronous activity induced by 4-aminopyridine in the juvenile rat hippocampus.

作者信息

Louvel J, Avoli M, Kurcewicz I, Pumain R

机构信息

Montreal Neurological Institute, McGill University, Que., Canada.

出版信息

Neurosci Lett. 1994 Feb 14;167(1-2):97-100. doi: 10.1016/0304-3940(94)91036-7.

Abstract

Field potential recordings and measurements of the extracellular concentration of free K+ ([K+]o) were made in the stratum radiatum of the CA3 subfield of hippocampal slices that were obtained from 12- to 17-day-old rats. Spontaneous, synchronous field potentials were recorded in the presence of the convulsant drug 4-aminopyridine (4AP, 50 microM). They consisted of interictal- (duration = 0.2-1.2 s; rate of occurrence = 0.3-1.3 Hz) and ictal-like epileptiform discharges (8-40 s; 4-38.10(-3) Hz), as well as large amplitude, negative-going potentials that preceded the onset of the ictal-like event. Such a temporal correlation suggested that the negative-going potential might facilitate the onset of ictal-like activity. Interictal- and ictal-like discharges were abolished by the AMPA/kainate receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 10 microM), while the negative-going potential was selectively blocked by bicuculline methiodide (BMI, 10 microM). Hence it was presumably due to the activation of GABAA receptors. [K+]o increased up to 12.5 mM (7.9 +/- 2.7 mM, mean +/- S.D.) from a resting value of 3.25 mM during the BMI-sensitive potentials (which also corresponded to the onset of ictal-like events), and after a decline to approximately 5 mM it remained elevated throughout the ictal event. Small, transient increases in [K+]o (up to 3.7 mM) could be seen during each interictal-like event. Following blockade of interictal- and ictal-like discharges by CNQX increases in [K+]o (up to 11 mM; 7.3 +/- 2.1; half-width = 7.2 +/- 2.3 s) still accompanied the BMI-sensitive negative-going potentials.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

对从12至17日龄大鼠获取的海马切片CA3亚区辐射层进行场电位记录和细胞外游离钾离子浓度([K+]o)测量。在惊厥药物4-氨基吡啶(4AP,50微摩尔)存在的情况下记录自发同步场电位。它们由发作间期(持续时间 = 0.2 - 1.2秒;发生率 = 0.3 - 1.3赫兹)和发作样癫痫样放电(8 - 40秒;4 - 38×10⁻³赫兹)以及发作样事件发作前的大幅度负向电位组成。这种时间相关性表明负向电位可能促进发作样活动的发作。AMPA/海人藻酸受体拮抗剂6-氰基-7-硝基喹喔啉-2,3-二酮(CNQX,10微摩尔)可消除发作间期和发作样放电,而甲硫酸荷包牡丹碱(BMI,10微摩尔)可选择性阻断负向电位。因此,推测这是由于GABAA受体的激活。在BMI敏感电位期间(这也与发作样事件的发作相对应),[K+]o从静息值3.25毫摩尔增加至12.5毫摩尔(7.9±2.7毫摩尔,平均值±标准差),在下降至约5毫摩尔后,在整个发作事件期间仍保持升高。在每个发作间期样事件期间可观察到[K+]o的小幅度短暂升高(高达3.7毫摩尔)。在CNQX阻断发作间期和发作样放电后,[K+]o的升高(高达11毫摩尔;7.3±2.1;半峰宽 = 7.2±2.3秒)仍伴随BMI敏感的负向电位。(摘要截断于250字)

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