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通过的轴突可能是小脑顶核升压反应的原因。

Axons of passage may be responsible for fastigial nucleus pressor response.

作者信息

Henry R T, Connor J D

机构信息

Department of Pharmacology, University of California, San Diego, La Jolla 92093.

出版信息

Am J Physiol. 1989 Dec;257(6 Pt 2):R1436-40. doi: 10.1152/ajpregu.1989.257.6.R1436.

Abstract

Bilateral destruction of perikarya in the fastigial nucleus (FN) of the rat with the cytotoxic agent kainic acid (0.5 mg) did not alter the blood pressure (BP) increases observed during monopolar electrical stimulation (100 microA, 50 Hz, 0.5-ms pulse width) of this region. BP increases in control animals were 30 +/- 8 mm Hg, whereas BP increased 30 +/- 7 mmHg in kainic acid-lesioned rats. Furthermore, picrotoxin (100 ng) and muscimol (25 ng) microinjected unilaterally into the FN of conscious, unrestrained rats produced postural asymmetry but no change in BP or heart rate. These data suggest that the FN pressor response may be due, at least in part, to stimulation of axons of passage.

摘要

用细胞毒性药物海人酸(0.5毫克)对大鼠小脑顶核(FN)的神经细胞体进行双侧破坏,并未改变在此区域进行单极电刺激(100微安、50赫兹、0.5毫秒脉冲宽度)时所观察到的血压(BP)升高。对照动物的血压升高为30±8毫米汞柱,而海人酸损伤的大鼠血压升高为30±7毫米汞柱。此外,向清醒、未束缚大鼠的FN单侧微量注射印防己毒素(100纳克)和蝇蕈醇(25纳克)会导致姿势不对称,但血压和心率无变化。这些数据表明,FN的升压反应可能至少部分是由于对通过的轴突的刺激所致。

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