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节后神经损伤后松果体的交感神经再支配不能恢复正常的松果体功能。

Sympathetic reinnervation of the pineal gland after postganglionic nerve lesion does not restore normal pineal function.

作者信息

Bowers C W, Baldwin C, Zigmond R E

出版信息

J Neurosci. 1984 Aug;4(8):2010-5. doi: 10.1523/JNEUROSCI.04-08-02010.1984.

Abstract

The activity of the enzyme serotonin N-acetyltransferase (NAT) in the rat pineal gland exhibits a large circadian rhythm, with peak activity occurring at night. This rhythm is dependent on stimulation of the pineal gland by neurons whose cell bodies are in the superior cervical ganglia and whose axons reach the gland via the internal carotid nerves (ICNs). Two days after both ICN were cut, crushed, or frozen, nighttime NAT activity was decreased by 90%. The remaining low level of enzyme activity was not affected by decentralization of the superior cervical ganglia. Thus, this enzyme activity did not depend on the activity of neurons in these ganglia. Bilaterally lesioning the ICN also abolished the neuronal uptake of norepinephrine in the pineal, further indicating that the sympathetic innervation of the gland had been destroyed. Three months after crushing both ICNs, nighttime NAT activity was only 20% of control values. However, in these animals, bilateral decentralization of the superior cervical ganglion reduced this low level of NAT activity by 90%. Thus, NAT activity, although low, was again dependent on sympathetic nerve stimulation. In contrast to this rather small recovery of nocturnal NAT activity, the norepinephrine uptake capacity of the gland recovered to 60% of control values. A similar discrepancy between the extent of recovery of NAT activity and of norepinephrine uptake was observed when the ICNs were frozen rather than crushed. To determine to what extent the sympathetic nerves that had reinnervated the pineal gland in these lesioned animals were capable of regulating NAT activity, their cervical sympathetic trunks were stimulated electrically at 5 Hz for 3 hr during the daytime.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

大鼠松果体中血清素N - 乙酰基转移酶(NAT)的活性呈现出较大的昼夜节律,夜间活性达到峰值。这种节律依赖于细胞体位于颈上神经节且轴突通过颈内神经(ICN)到达松果体的神经元对松果体的刺激。双侧颈内神经切断、挤压或冷冻两天后,夜间NAT活性降低了90%。剩余的低水平酶活性不受颈上神经节去神经支配的影响。因此,这种酶活性不依赖于这些神经节中神经元的活性。双侧损伤颈内神经也消除了松果体中去甲肾上腺素的神经元摄取,进一步表明该腺体的交感神经支配已被破坏。挤压双侧颈内神经三个月后,夜间NAT活性仅为对照值的20%。然而,在这些动物中,双侧颈上神经节去神经支配使这种低水平的NAT活性降低了90%。因此,NAT活性虽然较低,但再次依赖于交感神经刺激。与夜间NAT活性的这种相当小的恢复相比,腺体的去甲肾上腺素摄取能力恢复到对照值的60%。当颈内神经被冷冻而非挤压时,观察到NAT活性和去甲肾上腺素摄取恢复程度之间存在类似差异。为了确定在这些受损动物中重新支配松果体的交感神经在多大程度上能够调节NAT活性,在白天以5Hz的频率对其颈交感干进行3小时的电刺激。(摘要截断于250字)

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