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A1细胞群介导视上核加压素细胞的孤束核兴奋。

A1 cell group mediates solitary nucleus excitation of supraoptic vasopressin cells.

作者信息

Day T A, Sibbald J R

机构信息

Department of Physiology, University of Otago Medical School, Dunedin, New Zealand.

出版信息

Am J Physiol. 1989 Nov;257(5 Pt 2):R1020-6. doi: 10.1152/ajpregu.1989.257.5.R1020.

Abstract

Stimulation of the nucleus tractus solitarius (NTS) excites putative vasopressin-secreting cells of the supraoptic nucleus (SON) via a catecholaminergic projection to hypothalamus. Despite recent evidence of a direct catecholaminergic projection from NTS to SON, we have performed single-unit recording experiments in pentobarbital sodium-anesthetized rats to investigate the possibility that NTS stimulation effects on SON vasopressin cells are indirect, being relayed via the A1 noradrenergic cell group of the caudal ventrolateral medulla. The effects of single-pulse NTS and A1 region stimulation on the activity of antidromically identified SON neurosecretory cells that had been functionally characterized as vasopressin secreting were compared. NTS stimulation excited 81% of all putative vasopressin-secreting cells tested (n = 83), with a mean onset latency of 51 +/- 1 ms. A1 region stimulation excited 76% of all cells tested and 90% of units responsive to NTS stimulation, with a mean latency of 39 +/- 1 ms. Consistent with previous work NTS stimulation excited only a minority of oxytocin cells tested (3/13), and of these two-thirds also responded to A1 stimulation. Bilateral electrolytic lesions of the A1 region abolished the effects of NTS stimulation on putative vasopressin cells. Ipsilateral A1 region injections of the inhibitory neurotransmitter gamma-amino-butyric acid reversibly blocked NTS stimulation effects on putative vasopressin cells in animals where the contralateral A1 region had already been lesioned. These results support the proposal that excitation of SON vasopressin-secreting cells after NTS stimulation is due to activation of a relay projection through the A1 noradrenergic cell group of the caudal ventrolateral medulla.

摘要

刺激孤束核(NTS)可通过一条向下丘脑的儿茶酚胺能投射通路兴奋视上核(SON)中假定的血管加压素分泌细胞。尽管最近有证据表明存在从NTS到SON的直接儿茶酚胺能投射通路,但我们还是在戊巴比妥钠麻醉的大鼠身上进行了单单位记录实验,以研究NTS刺激对SON血管加压素细胞的影响是否是间接的,即通过延髓尾端腹外侧的A1去甲肾上腺素能细胞群进行中继。比较了单脉冲NTS和A1区刺激对经逆向鉴定且功能上已被确定为血管加压素分泌的SON神经分泌细胞活性的影响。NTS刺激使所有测试的假定血管加压素分泌细胞中的81%(n = 83)兴奋,平均起始潜伏期为51±1毫秒。A1区刺激使所有测试细胞中的76%以及对NTS刺激有反应的单位中的90%兴奋,平均潜伏期为39±1毫秒。与之前的研究一致,NTS刺激仅使少数测试的催产素细胞(3/13)兴奋,其中三分之二也对A1刺激有反应。A1区的双侧电解损伤消除了NTS刺激对假定血管加压素细胞的影响。在对侧A1区已经受损的动物中,同侧A1区注射抑制性神经递质γ-氨基丁酸可可逆地阻断NTS刺激对假定血管加压素细胞的影响。这些结果支持了这样一种观点,即NTS刺激后SON血管加压素分泌细胞的兴奋是由于通过延髓尾端腹外侧的A1去甲肾上腺素能细胞群的中继投射被激活所致。

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