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延髓头端腹外侧区的神经元介导躯体升压反射。

Neurons of rostral ventrolateral medulla mediate somatic pressor reflex.

作者信息

Stornetta R L, Morrison S F, Ruggiero D A, Reis D J

机构信息

Department of Neurology, Cornell University Medical College, New York, New York 10021.

出版信息

Am J Physiol. 1989 Feb;256(2 Pt 2):R448-62. doi: 10.1152/ajpregu.1989.256.2.R448.

Abstract

The somatic pressor reflex (SPR) elicited in anesthetized paralyzed rats by electrical stimulation of the sciatic or sural cutaneous afferent nerves produced an increase in arterial pressure ranging from 5 to 40 mmHg. Stimulation of femoral or tibial afferent nerves from muscle produced a depressor response. The SPR was not affected by midpontine transection but was eliminated either by hemisection of the lumbar spinal cord contralateral, but not ipsilateral, to the stimulated nerve or by electrolytic or kainic acid lesion of the contralateral, but not ipsilateral, rostral ventrolateral medulla (RVL). Stimulation of the brachial plexus elicited an SPR that was not eliminated by contralateral lumbar hemisection but was abolished by RVL lesion. RVL lesions consistently overlapped areas containing phenylethanolamine N-methyltransferase-labeled C1 adrenergic neurons. Kainic acid injections into the lateral reticular nucleus (LRN) did not affect the SPR. Neither contralateral nor ipsilateral electrolytic lesions of other autonomic areas including parabrachial nucleus, the nucleus tractus solitarii, the A5 region, or the inferior cerebellar peduncle (output pathway of the LRN) affected the reflex. In axonal transport studies using horseradish peroxidase, afferent terminals of the sciatic nerve were shown to overlap spinoreticular neurons in the dorsal horn retrogradely labeled from tracer injections in the RVL. We conclude that the SPR can be elicited in rats, that it is mediated by spinoreticular afferents traveling in the contralateral spinal cord, and that the C1 adrenergic area of the RVL is a critical region for the integration of the somatic pressor reflex.

摘要

在麻醉的瘫痪大鼠中,通过电刺激坐骨神经或腓肠皮神经引发的躯体升压反射(SPR)使动脉压升高5至40 mmHg。刺激来自肌肉的股神经或胫神经传入神经则产生降压反应。中脑桥中部横断不影响SPR,但通过对受刺激神经对侧(而非同侧)的腰脊髓半横断,或对侧(而非同侧)延髓头端腹外侧(RVL)的电解损伤或 kainic 酸损伤可消除SPR。刺激臂丛神经引发的SPR不会因对侧腰脊髓半横断而消除,但会因RVL损伤而消失。RVL损伤始终与含有苯乙醇胺N -甲基转移酶标记的C1肾上腺素能神经元的区域重叠。向外侧网状核(LRN)注射 kainic 酸不影响SPR。包括臂旁核、孤束核、A5区或小脑下脚(LRN的输出通路)在内的其他自主神经区域的对侧或同侧电解损伤均不影响该反射。在使用辣根过氧化物酶的轴突运输研究中,坐骨神经的传入终末显示与从RVL中的示踪剂注射逆行标记的背角中的脊髓网状神经元重叠。我们得出结论,SPR可在大鼠中引发,它由对侧脊髓中的脊髓网状传入神经介导,并且RVL的C1肾上腺素能区域是躯体升压反射整合的关键区域。

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