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神经降压素调节大鼠孤束核中的突触传递。

Neurotensin modulates synaptic transmission in the nucleus of the solitary tract of the rat.

作者信息

Ogawa W N, Baptista V, Aguiar J F, Varanda W A

机构信息

University of Tocantins, Porto Nacional/TO, Brazil.

出版信息

Neuroscience. 2005;130(2):309-15. doi: 10.1016/j.neuroscience.2004.09.019.

Abstract

Whole-cell patch clamp recordings were made from neurons of the rat subpostremal region of the nucleus tractus solitarius (NTS) in transverse brainstem slices. Neurotensin (NT) enhanced the firing rate of action potentials from 0.8 +/- 0.4 Hz in control to 1.9 +/- 1.3 Hz (n = 9) and increased their decay time. The peak amplitude of the after-hyperpolarization was decreased by 34+/-5% (n = 9). These effects were associated with a depolarization of 4 +/- 1 mV (n = 10) in the resting membrane potential and an increase in the input resistance (from 768 +/- 220 MOmega to 986+/-220 MOmega; n = 5) and were compensated by manually hyperpolarizing the cell to control values. In voltage clamp experiments NT decreased an outward current (from 488 +/- 161 to 340 +/- 96 pA at +40 mV; n = 5) which reversed near the potassium equilibrium potential. In addition, NT increased the frequency of both excitatory and inhibitory spontaneous synaptic currents, an effect blocked by tetrodotoxin, and did not change the evoked excitatory or inhibitory postsynaptic currents. The selective NTR1 receptor antagonist SR48692 reversibly blocked the effects of NT on both action potentials and spontaneous synaptic currents. Our results suggest that NTR1 receptors can modulate post-synaptic responses in neurons of the subpostremal NTS by increasing cell excitability as a result of blockade of a potassium conductance.

摘要

在横断脑干切片中,对大鼠孤束核(NTS)后极下区域的神经元进行全细胞膜片钳记录。神经降压素(NT)将动作电位的发放频率从对照时的0.8±0.4Hz提高到1.9±1.3Hz(n = 9),并增加了其衰减时间。超极化后电位的峰值幅度降低了34±5%(n = 9)。这些效应与静息膜电位去极化4±1mV(n = 10)以及输入电阻增加(从768±220MΩ增加到986±220MΩ;n = 5)有关,并且通过手动将细胞超极化至对照值来进行补偿。在电压钳实验中,NT降低了外向电流(在+40mV时从488±161pA降至340±96pA;n = 5),该电流在钾平衡电位附近反转。此外,NT增加了兴奋性和抑制性自发突触电流的频率,这一效应被河豚毒素阻断,并且NT不改变诱发的兴奋性或抑制性突触后电流。选择性NTR1受体拮抗剂SR48692可逆地阻断了NT对动作电位和自发突触电流的影响。我们的结果表明,NTR1受体可通过阻断钾电导增加细胞兴奋性,从而调节后极下NTS神经元的突触后反应。

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