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豚鼠和猫丘脑神经元放电模式的去甲肾上腺素能调制,体外研究。

Noradrenergic modulation of firing pattern in guinea pig and cat thalamic neurons, in vitro.

作者信息

McCormick D A, Prince D A

机构信息

Department of Neurology, Stanford University School of Medicine, California 94305.

出版信息

J Neurophysiol. 1988 Mar;59(3):978-96. doi: 10.1152/jn.1988.59.3.978.

Abstract
  1. The electrophysiological actions of norepinephrine (NE) in the guinea pig and cat thalamus were investigated using intracellular recordings from neurons of in vitro thalamic slices. 2. Application of NE to neurons of the lateral and medial geniculate nuclei, nucleus reticularis, anteroventral nucleus, and the parataenial (PT) nucleus resulted in a slow depolarization associated with a 2- to 15-nS decrease in input conductance and an increase in the slow membrane time constant from an average of 27.7 to 37.7 ms. The slow depolarization was not abolished by blockade of synaptic transmission, indicating that it was a direct (postsynaptic) effect. 3. The reversal potential of the NE-induced slow depolarization varied as a Nernstian function of extracellular potassium concentration ([K]o), indicating that it is due to a decrease in potassium conductance. This conclusion was supported by the finding that the amplitude of the NE-evoked depolarization was affected by changes in [K]o between 0.5 and 5.0 mM as expected for a K-mediated response. 4. Neurons of the PT nucleus displayed unusually large afterhyperpolarizations (AHPs) in comparison to cells in other thalamic nuclei. NE application to PT neurons caused not only a marked slow depolarization and decreased conductance, but also selectively reduced the slow AHP. 5. The NE-induced slow depolarization effectively suppressed burst firing and promoted the occurrence of single spike activity. NE-induced reduction of the slow AHP in PT neurons was accompanied by a decrease in spike frequency accommodation and the emergence of a slow afterdepolarization. 6. We suggest that through these electrophysiological actions, NE can effectively inhibit the generation of thalamocortical rhythms and greatly facilitate the faithful transfer of information through the thalamus to the cerebral cortex.
摘要
  1. 利用体外丘脑切片神经元的细胞内记录,研究了去甲肾上腺素(NE)在豚鼠和猫丘脑中的电生理作用。2. 将NE施加于外侧和内侧膝状体核、网状核、前腹核以及旁束旁(PT)核的神经元,导致缓慢去极化,同时输入电导降低2至15纳西门子,慢膜时间常数从平均27.7毫秒增加到37.7毫秒。突触传递阻断并未消除这种缓慢去极化,表明这是一种直接(突触后)效应。3. NE诱导的缓慢去极化的反转电位随细胞外钾浓度([K]o)呈能斯特函数变化,表明其是由于钾电导降低所致。这一结论得到以下发现的支持:如预期的钾介导反应一样,在0.5至5.0毫摩尔之间的[K]o变化会影响NE诱发的去极化幅度。4. 与其他丘脑核中的细胞相比,PT核的神经元表现出异常大的超极化后电位(AHPs)。将NE施加于PT神经元不仅导致明显的缓慢去极化和电导降低,还选择性地减小了缓慢的AHP。5. NE诱导的缓慢去极化有效抑制了爆发式放电并促进了单峰活动的发生。NE诱导的PT神经元缓慢AHP的降低伴随着放电频率适应性的降低和缓慢去极化后的出现。6. 我们认为,通过这些电生理作用,NE可以有效抑制丘脑皮质节律的产生,并极大地促进信息通过丘脑向大脑皮质的可靠传递。

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