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细胞内刺激诱发的小脑浦肯野神经元中的钙瞬变。

Calcium transients in cerebellar Purkinje neurons evoked by intracellular stimulation.

作者信息

Lev-Ram V, Miyakawa H, Lasser-Ross N, Ross W N

机构信息

Department of Physiology, New York Medical College, Valhalla 10595.

出版信息

J Neurophysiol. 1992 Oct;68(4):1167-77. doi: 10.1152/jn.1992.68.4.1167.

Abstract
  1. Purkinje cells in thin slices from the guinea pig cerebellum were injected with fura-2 and high-speed sequences of fluorescence images from the cell body and entire dendritic tree were made while simultaneously recording somatic membrane potential during evoked and spontaneous electrical activity. The changes in fluorescence were interpreted in terms of changes in [Ca2+]i. 2. Individual calcium action potentials were usually accompanied by transient increases in [Ca2+]i all over the dendritic field. During evoked or spontaneous bursts of calcium spikes, [Ca2+]i increased more rapidly and to higher concentrations in fine dendrites than in thicker dendrites. At the end of a burst [Ca2+]i declined faster in thin dendrites than in thicker ones. These variations are most easily understood as deriving from the difference in surface-to-volume ratio of the two kinds of dendrites. 3. During bursts of calcium action potentials [Ca2+]i increases sometimes occurred only in individual dendritic branches, but always including the fine dendrites of that particular branch, showing that calcium action potentials can be regenerative in restrictive parts of the dendritic field without involving the soma or dendritic shaft. 4. Plateau or subthreshold potential changes evoked in the presence of tetrodotoxin (TTX) caused small, widespread increases in [Ca2+]i. The amplitude of these changes was much less than the increase corresponding to spike bursts. The distribution of these plateau Ca signals in thick and thin dendrites was similar to Ca spike-evoked signals, suggesting that the Ca conductances underlying these two potentials are the same or are distributed similarly in the dendrites. 5. Significant increases in [Ca2+]i in the soma were recorded during bursts of sodium-dependent action potentials in normal Ringer. Although much of this increase is due to calcium entry through calcium channels, some of this increase could be due to calcium entry through sodium channels.
摘要
  1. 用fura - 2对豚鼠小脑薄片中的浦肯野细胞进行注射,并在诱发和自发电活动期间同时记录体细胞动作电位时,获取细胞体和整个树突树的高速荧光图像序列。荧光变化根据细胞内钙离子浓度([Ca2+]i)的变化来解释。2. 单个钙动作电位通常伴随着整个树突区域内[Ca2+]i的瞬时增加。在诱发或自发的钙峰发放期间,细树突中[Ca2+]i的增加比粗树突更快且浓度更高。在发放结束时,细树突中[Ca2+]i的下降比粗树突更快。这些差异最容易理解为源自两种树突的表面积与体积比的不同。3. 在钙动作电位发放期间,[Ca2+]i的增加有时仅发生在单个树突分支中,但总是包括该特定分支的细树突,这表明钙动作电位可以在树突区域的特定部位再生,而不涉及细胞体或树突干。4. 在存在河豚毒素(TTX)的情况下诱发的平台电位或阈下电位变化会导致[Ca2+]i出现小范围的普遍增加。这些变化的幅度远小于与峰发放相对应的增加幅度。这些平台钙信号在粗树突和细树突中的分布与钙峰诱发信号相似,表明这两种电位所依赖的钙电导相同或在树突中分布相似。5. 在正常林格氏液中,钠依赖性动作电位发放期间记录到细胞体中[Ca2+]i显著增加。虽然这种增加大部分是由于钙通过钙通道进入细胞,但其中一些增加可能是由于钙通过钠通道进入细胞。

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