Leptin Modulates Spike Coding in the Rat Suprachiasmatic Nucleus
Leptin Modulates Spike Coding in the Rat Suprachiasmatic Nucleus
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DOI：
10.1111/j.1365-2826.2009.01889.x
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发表时间：
2009-08-01
影响因子：
3.2
通讯作者：
Dyball, R. E. J.
中科院分区：
文献类型：
--
作者：
Inyushkin, A. N.;Bhumbra, G. S.;Dyball, R. E. J.
哺乳动物的昼夜节律起搏器--视交叉上核（SCN）含有脂肪组织激素瘦素的受体。在本研究中，瘦素对SCN细胞的电生理活性的影响，其特征在于在体外大鼠脑切片。在细胞外记录过程中，应用20 nm瘦素（n = 36）降低了平均峰频率（Wilcoxon符号秩检验，z =-3.390，P < 0.001），并增加了由对数峰间期分布熵测量的放电不规则性（Student配对t检验，t = 2.377，P = 0.023），但对通过相邻对数峰间期之间的互信息测量的峰图案没有一致的影响（z = 0.745，P = 0.456）。细胞内电流钳记录（n = 25）显示20 nm瘦素对SCN神经元具有超极化作用（z =-2.290，P = 0.022）。超极化主要是由于瘦素对细胞亚组（n = 13）的作用，其在超极化电流脉冲终止时产生“反弹”尖峰（z =-2.697，P = 0.007）。应用瘦素也增加了组平均后超极化持续时间（n = 25，t = 2.512，P = 0.023）。瘦素对细胞外记录的锋电位的影响与膜电位和锋电位形状的变化一致。他们认为，瘦素可以直接调节SCN神经元的电特性，并以这种方式，有助于代谢过程影响生物钟的机制。
The mammalian circadian pacemaker, the suprachiasmatic nucleus (SCN), contains receptors to the adipose tissue hormone leptin. In the present study, the effects of leptin on the electrophysiological activity of the SCN cells were characterised in vitro in rat brain slices. During extracellular recording, application of 20 nm leptin (n = 36) decreased mean spike frequency (Wilcoxon signed rank test, z = -3.390, P < 0.001) and increased the irregularity of firing measured by the entropy of the log interspike interval distribution (Student's paired t-test, t = 2.377, P = 0.023), but had no consistent effect on spike patterning as measured by the mutual information between adjacent log interspike intervals (z = 0.745, P = 0.456). Intracellular current-clamp recordings (n = 25) revealed a hyperpolarising effect of 20 nm leptin on SCN neurones (z = -2.290, P = 0.022). The hyperpolarisation largely resulted from the effect of leptin on the subgroup of cells (n = 13) that generated 'rebound' spikes upon termination of a hyperpolarising current pulse (z = -2.697, P = 0.007). Leptin application also increased the group mean duration of the afterhyperpolarisation (n = 25, t = 2.512, P = 0.023). The effects of leptin on extracellularly recorded spike activity were consistent with the changes in membrane potential and spike shape. They suggest that leptin can directly modulate the electrical properties of SCN neurones and, in this way, contribute to the mechanism by which metabolic processes influence the circadian clock.