Neuropeptide Y and catecholamine synthesizing enzymes and their mRNAs in rat sympathetic neurons and adrenal glands: studies on expression, synthesis and axonal transport after pharmacological and experimental manipulations using hybridization techniques
Neuropeptide Y and catecholamine synthesizing enzymes and their mRNAs in rat sympathetic neurons and adrenal glands: studies on expression, synthesis and axonal transport after pharmacological and experimental manipulations using hybridization techniques
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大鼠交感神经元和肾上腺中的神经肽 Y 和儿茶酚胺合成酶及其 mRNA：使用杂交技术进行药理学和实验操作后的表达、合成和轴突运输的研究
DOI：
10.1016/0306-4522(91)90365-u
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发表时间：
1991
期刊：
影响因子：
3.3
通讯作者：
Lundberg,JM
中科院分区：
文献类型：
--
作者：
Schalling,M;Franco-Cereceda,A;Hemsén,A;Dagerlind,A;Seroogy,K;Persson,H;Hökfelt,T;Lundberg,JM
比较利血平治疗（10 mg/kg, ig）对大鼠交感神经元和肾上腺中神经肽Y、酪氨酸羟化酶和苯乙醇胺甲基转移酶mRNA编码水平和儿茶酚胺含量的影响。右心房心脏、肾脏和咬肌的神经肽Y样免疫反应性可逆性减弱，而星状神经节和腰交感神经节的免疫反应性神经肽Y含量及其在坐骨神经的轴突转运增加。星状神经节的增加在利血平治疗后48 h达到最大，在第9天消失。星状神经节和颈上神经节中神经肽Y mRNA和酪氨酸羟化酶mRNA的表达比神经肽Y含量的升高早，在利血平作用后24 h明显升高2倍。在烟碱受体拮抗剂（氯异丹明）和手术神经节前去神经支配治疗后，上颈神经节两种mrna的增加和末梢区域神经肽Y的消耗（但不包括去甲肾上腺素）被阻止。在利血平治疗24小时后，肾上腺中神经肽Y样免疫反应性和肾上腺素明显（75-90%）降低，同时神经肽Y mRNA和酪氨酸羟化酶mRNA表达增加3 - 4倍。同样在肾上腺中，利血平诱导的神经肽Y mRNA和酪氨酸羟化酶mRNA的增加和神经肽Y和肾上腺素的消耗在内脏去神经支配后发生逆转。药理学上，神经节阻滞能抑制神经肽Y的消耗和神经肽Y mRNA表达的增加，但不能完全抑制酪氨酸羟化酶mRNA的升高。此外，利血平治疗后苯乙醇胺-甲基转移酶emrna水平显著降低。这种减少被去神经支配和神经节阻滞逆转。单独去神经支配导致颈上神经节和肾上腺髓质中所有mrna的少量但显著减少。目前的数据表明，利血平后交感神经和肾上腺中神经肽Y样免疫反应性的减少与神经肽Y合成和轴突转运代偿性增加有关，这很可能是由于尼古丁受体刺激增加所致。尽管交感神经和肾上腺中神经肽Y的利血平耗竭与神经元激活有关，但儿茶酚胺在肾上腺而非神经末端的耗竭可以通过神经节阻滞剂氯异旦胺来预防。神经节阻滞对肾上腺髓质神经肽Y mRNA和酪氨酸羟化酶mRNA影响的差异提示，除乙酰胆碱外，可能还有其他信使参与酪氨酸羟化酶的调控。最后，酪氨酸羟化酶mRNA和苯乙醇胺甲基转移酶mRNA似乎至少部分地通过不同的神经元机制进行调节。
The effects of reserpine treatment (10 mg/kg, i.p.) on the content of neuropeptide Y-like immunoreactivity and catecholamines were compared with the levels of mRNA coding for neuropeptide Y, tyrosine hydroxylase and phenylethanolamineN-methyltransferasein rat sympathetic neurons and adrenal gland. A reversible depletion of neuropeptide Y-like immunoreactivity was observed in the right atrium of the heart, kidney and masseter muscle, while the immunoreactive neuropeptide Y content in the stellate and lumbar sympathetic ganglia and its axonal transport in the sciatic nerve increased following reserpine. The increase in the stellate ganglion was maximal at 48 h and absent 9 days after reserpine treatment.The expression of neuropeptide Y mRNA and tyrosine hydroxylase mRNA in both the stellate and the superior cervical ganglion increased earlier than the neuropeptide Y content, with a clear cut two-fold elevation at 24 h after reserpine. The increase in both mRNAs in the superior cervical ganglion and the depletion of neuropeptide Y, but not of noradrenaline, in terminal areas was prevented after pretreatment both with a nicotinic receptor antagonist (chlorisondamine) and with surgical preganglionic denervation.A marked (75–90%) depletion of neuropeptide Y-like immunoreactivity and adrenaline in the adrenal gland, concomitant with 3–4-fold increases in neuropeptide Y mRNA and tyrosine hydroxylase mRNA expression, was present at 24 h after reserpine treatment. Also in the adrenal gland, there was a reversal of the reserpine-induced increase in neuropeptide Y mRNA and tyrosine hydroxylase mRNA and depletion of neuropeptide Y and adrenaline following splanchnic denervation. Pharmacological, ganglionic blockade prevented the depletion of neuropeptide Y and the increased expression of neuropeptide Y mRNA, but not fully, the tyrosine hydroxylase mRNA elevation. In addition, a marked decrease in phenylethanolamineN-methyltransferasemRNA levels was noted after reserpine. This decrease was reversed by denervation and by ganglionic blockade. Denervation alone led to a small but significant decrease in all mRNAs examined both in the superior cervical ganglion and the adrenal medulla.The present data suggest that the depletion of neuropeptide Y-like immunoreactivity in sympathetic nerves and in the adrenal gland after reserpine is associated with a compensatory increase in neuropeptide Y synthesis and axonal transport, most likely due to increased nicotinic receptor stimulation. Whereas the reserpine depletion of neuropeptide Y in both sympathetic nerves and adrenal gland is related to neuronal activation, adrenal but not nerve terminal depletion of catecholamines can be prevented by the ganglionic blocker chlorisondamine. The difference in effect of pharmacological ganglionic blockade on neuropeptide Y mRNA and tyrosine hydroxylase mRNA in the adrenal medulla suggests that other messengers than acetylcholine may be involved in regulation of tyrosine hydroxylase. Finally, tyrosine hydroxylase mRNA and phenylethanolamineN-methyltransferasemRNA appear to be regulated at least partly via separate neuronal mechanisms.
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影响因子：
3.5
作者：
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通讯作者：
M. Laposata
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DOI：
--
发表时间：
2006
期刊：
Alcohol Research and Health
影响因子：
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DOI：
10.2146/ajhp060644
发表时间：
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期刊：
American journal of health-system pharmacy : AJHP : official journal of the American Society of Health-System Pharmacists
影响因子：
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DOI：
10.3390/ijerph7124281
发表时间：
2010-12
影响因子：
--
作者：
Manzo-Avalos S;Saavedra-Molina A
通讯作者：
Saavedra-Molina A
影响因子：
13.5
作者：
Zhang, Yingmei;Ren, Jun
通讯作者：
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