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单胺能通路对交感神经节前神经元的功能作用。

Functional roles of monoaminergic pathways to sympathetic preganglionic neurons.

作者信息

Franz D N, Madsen P W, Peterson R G, Sangdee C

出版信息

Clin Exp Hypertens A. 1982;4(4-5):543-62. doi: 10.3109/10641968209061598.

DOI:10.3109/10641968209061598
PMID:6286173
Abstract

Despite considerable progress in mapping the central monoaminergic pathways to sympathetic preganglionic neurons in the spinal cord, the respective functional roles of these pathways have not been resolved. Evidence for both excitation and inhibition has been advanced for each of the three monoamines, serotonin, norepinephrine, and epinephrine. Our previous studies on spinal sympathetic pathways to sympathetic preganglionic neurons support the prevailing opinion that serotonin pathways are inhibitory but did not satisfactorily resolve the functional role of the norepinephrine pathways. However, more recent studies showing that intraspinally evoked sympathetic discharges were rapidly and markedly enhanced by phosphodiesterase inhibitors and that this effect was prevented by clonidine have led to formulation of a coherent hypothesis which accommodates much of the conflicting evidence regarding norepinephrine. In addition, evidence for the role of the epinephrine pathways has been obtained by using a selective inhibitor of epinephrine synthesis. The results of these recent studies complement our previous results and suggest that the excitability of sympathetic preganglionic neurons is regulated by excitatory norepinephrine pathways and inhibitory epinephrine pathways that activate or suppress adenylate cyclase to control intraneuronal levels of cyclic AMP.

摘要

尽管在绘制脊髓中向交感神经节前神经元投射的中枢单胺能通路方面取得了显著进展,但这些通路各自的功能作用尚未明确。对于三种单胺(5-羟色胺、去甲肾上腺素和肾上腺素)中的每一种,都有兴奋和抑制的相关证据。我们之前对脊髓通向交感神经节前神经元的交感通路的研究支持了一种普遍观点,即5-羟色胺通路具有抑制作用,但未能令人满意地阐明去甲肾上腺素通路的功能作用。然而,最近的研究表明,磷酸二酯酶抑制剂可迅速且显著增强脊髓内诱发的交感神经放电,且可乐定可阻止这种效应,这导致了一个连贯假说的形成,该假说涵盖了许多关于去甲肾上腺素的相互矛盾的证据。此外,通过使用肾上腺素合成的选择性抑制剂,已获得了关于肾上腺素通路作用的证据。这些最新研究结果补充了我们之前的研究结果,并表明交感神经节前神经元的兴奋性受兴奋性去甲肾上腺素通路和抑制性肾上腺素通路的调节,这些通路通过激活或抑制腺苷酸环化酶来控制神经元内的环磷酸腺苷水平。

相似文献

1
Functional roles of monoaminergic pathways to sympathetic preganglionic neurons.单胺能通路对交感神经节前神经元的功能作用。
Clin Exp Hypertens A. 1982;4(4-5):543-62. doi: 10.3109/10641968209061598.
2
Enhancement of central transmission to sympathetic preganglionic neurons by phosphodiesterase inhibitors and its prevention by clonidine.磷酸二酯酶抑制剂增强对交感神经节前神经元的中枢传递及其被可乐定阻断的作用
J Auton Nerv Syst. 1987 Jun;19(3):199-209. doi: 10.1016/0165-1838(87)90066-x.
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Evidence for inhibition of sympathetic preganglionic neurons by bulbospinal epinephrine pathways.
Neurosci Lett. 1983 Jun 16;37(2):167-73. doi: 10.1016/0304-3940(83)90148-9.
4
Clonidine prevents enhancement of spinal sympathetic transmission by phosphodiesterase inhibitors.可乐定可防止磷酸二酯酶抑制剂增强脊髓交感神经传递。
Neurosci Lett. 1982 Feb 12;28(2):211-6. doi: 10.1016/0304-3940(82)90154-9.
5
Inhibition of the activity of sympathetic preganglionic neurones and neurones activated by visceral afferents, by alpha-methylnoradrenaline and endogenous catecholamines.
Neuropharmacology. 1983 Jan;22(1):3-17. doi: 10.1016/0028-3908(83)90255-1.
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Monoaminergic modulation of spinal viscero-sympathetic function in the neonatal mouse thoracic spinal cord.单胺能调制新生鼠胸段脊髓内脏-交感功能。
PLoS One. 2012;7(11):e47213. doi: 10.1371/journal.pone.0047213. Epub 2012 Nov 5.
7
L-dopa-induced hypotension: depression of spinal sympathetic neurons by release of 5-hydroxytryptamine.
Adv Exp Med Biol. 1977;90:219-232. doi: 10.1007/978-1-4684-2511-6_13.
8
Depression of sympathetic preganglionic neurons by clonidine: evidence for stimulation of 5-HT receptors.可乐定对交感神经节前神经元的抑制作用:5-羟色胺受体受刺激的证据
Clin Exp Hypertens (1978). 1978;1(1):115-40. doi: 10.3109/10641967809068599.
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The role of descending monoaminergic systems in central control of blood pressure.下行单胺能系统在血压中枢控制中的作用。
Fed Proc. 1981 Nov;40(13):2778-85.
10
Glutamate- and GABA-immunoreactive synapses on sympathetic preganglionic neurons caudal to a spinal cord transection in rats.大鼠脊髓横断后尾侧交感神经节前神经元上的谷氨酸和γ-氨基丁酸免疫反应性突触。
Neuroscience. 1997 Oct;80(4):1225-35. doi: 10.1016/s0306-4522(97)00155-3.

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