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5-羟色胺2受体对猫延髓呼吸神经元的调控作用

5-HT2 receptor-controlled modulation of medullary respiratory neurones in the cat.

作者信息

Lalley P M, Bischoff A M, Schwarzacher S W, Richter D W

机构信息

Department of Physiology, University of Wisconsin Medical Science Center, Madison 53706, USA.

出版信息

J Physiol. 1995 Sep 15;487 ( Pt 3)(Pt 3):653-61. doi: 10.1113/jphysiol.1995.sp020907.

Abstract
  1. The effects of the 5-HT2 receptor agonist alpha-methyl-5-HT were studied on the membrane of expiratory (E2) and post-inspiratory (PI) neurones, by intracellular recordings in the caudal medulla of anaesthetized cats. 2. Ionophoresis of alpha-Me-5-HT depolarized membrane potential and increased action potential frequency in a majority of neurones tested. Depolarization of neurones by alpha-Me-5-HT was accompanied by increased input resistance throughout all phases of the respiratory cycle. These effects were antagonized by ionophoresis of cinanserin, a receptor-blocking agent with high affinity for 5-HT2 receptors. 3. E2 neurones were voltage clamped to measure membrane current changes induced by alpha-Me-5-HT ionophoresis. alpha-Me-5-HT induced a net inward current by reducing inspiratory-phase outward currents and increasing expiratory-phase inward currents. These changes were equivalent with steady membrane depolarization, decreased inspiratory phase membrane hyperpolarization and increased expiratory drive potential recorded from the same neurones in current clamp. 4. The effects of alpha-Me-5-HT are consistent with activation of 5-HT2 receptors on E2 and PI neurones leading to blockade of synaptically activated and persistent conductances to potassium ions.
摘要
  1. 通过对麻醉猫延髓尾部进行细胞内记录,研究了5-羟色胺2(5-HT2)受体激动剂α-甲基-5-羟色胺对呼气(E2)神经元和吸气后(PI)神经元膜的作用。2. 在大多数被测试的神经元中,α-甲基-5-羟色胺的离子电泳使膜电位去极化并增加动作电位频率。α-甲基-5-羟色胺引起的神经元去极化在呼吸周期的所有阶段都伴随着输入电阻的增加。这些效应被cinanserin(一种对5-HT2受体具有高亲和力的受体阻断剂)的离子电泳所拮抗。3. 对E2神经元进行电压钳制,以测量α-甲基-5-羟色胺离子电泳引起的膜电流变化。α-甲基-5-羟色胺通过减少吸气相外向电流和增加呼气相内向电流诱导净内向电流。这些变化与在电流钳中从同一神经元记录到的稳定膜去极化、吸气相膜超极化减少和呼气驱动电位增加相当。4. α-甲基-5-羟色胺的作用与E2和PI神经元上5-HT2受体的激活一致,导致对钾离子的突触激活和持续性电导的阻断。

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