L-DOPAergic components in the caudal ventrolateral medulla in baroreflex neurotransmission
L-DOPAergic components in the caudal ventrolateral medulla in baroreflex neurotransmission
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DOI：
10.1016/s0306-4522(98)00721-0
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发表时间：
1999-01-01
期刊：
影响因子：
3.3
通讯作者：
Misu, Y
中科院分区：
文献类型：
--
作者：
Miyamae, T;Goshima, Y;Misu, Y
L-3，4-二羟基苯丙氨酸(L-DOPA)可能是终止于孤束核的初级压力感受性传入的一种递质，L-DOPA的强直作用是激活延髓尾侧腹外侧区的降压点，后者接受孤束核的输入。(1996)青蛙。神经比奥。49,415-454]。我们试图阐明延髓尾侧腹外侧区的L-多巴胺能成分是否参与麻醉大鼠的压力感受性神经传递。右侧孤束核的电解性损害(1 mA DC。10a，测量前10d)选择性地将同侧延髓尾侧腹外侧区L多巴的组织含量降低45%。电解性损伤不会降低多巴胺、去甲肾上腺素和肾上腺素水平。在对右侧延髓尾侧腹外侧区进行微透析的过程中，用高效液相色谱-电化学检测法可检测到胞外L多巴、去甲肾上腺素、肾上腺素和3，4-二羟基苯乙酸的含量。然而，胞外多巴胺水平低于检测限值。静脉注射激活压力感受器。去甲肾上腺素选择性地诱发L-多巴酚胺，而不增加去甲肾上腺素、肾上腺素和3，4-二羟基苯乙酸的水平。急性损毁同侧孤束核可抑制L-多巴酚A的释放。间歇刺激右主动脉降压神经(20 Hz，3V，0.3ms，持续30min)可引起L多巴释放、低血压和心动过缓，但不增加去甲肾上腺素、肾上腺素和3，4-二羟基苯乙酸的水平。向同侧延髓尾侧腹外侧区注入30mU L-甲基-对酪氨酸局部抑制L-多巴的合成，可使L-多巴和3，4-二羟基苯乙酸的基础含量逐渐降低，而去甲肾上腺素和肾上腺素的含量无明显变化。抑制L-多巴合成可阻断L-多巴的释放，并使刺激主动脉神经引起的降压反应降低65%，但对心动过缓无影响。将主要的突触前抑制传递标志物CoCl2(119 Ng)和竞争性的L多巴受体拮抗剂L多巴甲酯(11 MU G)微量注射到右侧延髓尾侧腹外侧区的降压点，可使刺激同侧主动脉神经(20 Hz，3V，0.1ms，持续10 S)的降压反应降低60%。孤束核可能存在L-多巴胺能神经传递至延髓尾侧腹外侧区。大鼠延髓尾侧腹外侧区的L能成分通过压力感受器-降主动脉降压神经-孤束核-延髓尾侧腹外侧区的中继参与压力感受性神经传递。(C)1999年IBRO。爱思唯尔科学有限公司出版。
L-3,4-Dihydroxyphenylalanine (L-DOPA) is probably a transmitter of the primary baroreceptor afferents terminating in the nucleus tractus solitarii; L-DOPA functions tonically to activate depressor sites of the caudal ventrolateral medulla, which receives input from the nucleus tractus solitarii [Misu Y. et al. (1996) Frog. Neurobiol. 49, 415-454]. We have attempted to clarify whether or not L-DOPAergic components within the caudal ventrolateral medulla are involved in baroreflex neurotransmission in anesthetized rats. Electrolytic lesions of the right nucleus tractus solitarii (1 mA d.c. for 10 a, 10 days before measurement) selectively decreased by 45% the tissue content of L-DOPA in the dissected ipsilateral caudal ventrolateral medulla. Electrolytic lesions did not decrease dopamine, norepinephrine and epinephrine levels. During microdialysis of the right caudal ventrolateral medulla, extracellular levels of L-DOPA, norepinephrine, epinephrine and 3,4-dihydroxyphenylacetic acid were consistently detectable using high-performance liquid chromatography with electrochemical detection. However, extracellular dopamine levels were lower than the assay limit. Baroreceptor activation by i.v. phenylephrine selectively evoked L-DOPA without increasing the levels of norepinephrine, epinephrine and 3,4-dihydroxyphenylacetic acid. This L-DOPA release was suppressed by acute lesion in the ipsilateral nucleus tractus solitarii. Intermittent stimulation of the right aortic depressor nerve (20 Hz, 3 V, 0.3 ms duration, for 30 min) repetitively and constantly caused L-DOPA release, hypotension and bradycardia, without increases in levels of norepinephrine, epinephrine and 3,4-dihydroxyphenylacetic acid. Local inhibition of L-DOPA synthesis with ol-methyl-p-tyrosine (30 mu M) infused into the ipsilateral caudal ventrolateral medulla gradually decreased basal levels of L-DOPA and 3,4-dihydroxyphenylacetic acid without decreasing norepinephrine and epinephrine. The inhibition of L-DOPA synthesis interrupted L-DOPA release and decreased by 65% depressor responses elicited by aortic nerve stimulation; however, it produced no effect on bradycardic responses. CoCl2 (119 ng), a mainly presynaptic inhibitory transmission marker, and L-DOPA methyl ester (1 1 mu g), a competitive L-DOPA antagonist, when microinjected into depressor sites of the right caudal ventrolateral medulla, reduced by 60% depressor responses to transient ipsilateral stimulation of the aortic nerve (20 Hz, 3 V, 0.1 ms duration, for 10 s). No changes in bradycardic responses were observed.There may exist an L-DOPAergic relay from the nucleus tractus solitarii to the caudal ventrolateral medulla. L-DOPAergic components in the caudal ventrolateral medulla are involved in baroreflex neurotransmission via a baroreceptor-aortic depressor nerve-nucleus tractus solitarii-caudal ventrolateral medulla relay in the rat. (C) 1999 IBRO. Published by Elsevier Science Ltd.