ACETYLCHOLINESTERASE STAINING AND CHOLINE-ACETYLTRANSFERASE ACTIVITY IN THE YOUNG-ADULT RAT SPLEEN - LACK OF EVIDENCE FOR CHOLINERGIC INNERVATION

ACETYLCHOLINESTERASE STAINING AND CHOLINE-ACETYLTRANSFERASE ACTIVITY IN THE YOUNG-ADULT RAT SPLEEN - LACK OF EVIDENCE FOR CHOLINERGIC INNERVATION
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DOI:
10.1006/brbi.1993.1021
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发表时间:
1993-09-01
影响因子:
15.1
通讯作者:
FELTEN, DL
FELTEN, DL
中科院分区:
医学1区
文献类型:
--
作者:
BELLINGER, DL;LORTON, D;FELTEN, DL

文献摘要

被引文献

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采用几种去神经模式,对青年sd大鼠脾脏进行乙酰胆碱酯酶(AChE)染色,以确定其脾AChE +神经纤维的来源。在所有对照组的脾脏中,沿脉管系统和小梁内均存在AChE +神经样谱。在脾脏淋巴样细胞和网状细胞以及肠系膜-腹腔上神经节(SM-CG)的神经元细胞体中也存在AChE +反应性。神经化学分析显示,对照动物脾脏胆碱乙酰转移酶活性不显著。手术切除SM-CG导致去甲肾上腺素能(NA)和AChE +神经图谱的完全丧失,以及脾脏非神经腔室AChE染色的丧失。在治疗后第1天和第3天,6-羟基多巴胺化学交感神经切除术也导致脾脏NA和AChE神经谱的丢失,除了肝门区少量抗性纤维。非神经室的乙酰胆碱酯酶反应性在脾的化学失神经区也减弱。化学交感神经切除术后10 ~ 56天,神经和非神经剖面的AChE染色逐渐增加,其时间过程和分布模式与NA纤维再支配脾脏相似。双侧迷走神经横断后保留AChE +染色。脾脏胆碱乙酰转移酶水平极低,表明充其量只有少量胆碱能神经分布于大鼠脾脏。此外,存在的胆碱能神经支配并不像早期文献中提出的那样来自迷走神经。总的来说,脾脏中AChE +和NA神经谱的重叠分布以及手术和化学交感神经切除术后神经纤维群的平行丢失支持了AChE在NA神经中与去甲肾上腺素共定位的存在,从而使AChE +染色成为大鼠脾脏胆碱能神经支配的不合适标记。
Acetylcholinesterase (AChE) staining in spleens from young adult Sprague–Dawley rats was examined following several denervation paradigms to determine the source of splenic AChE + nerve fibers. In spleens from all control groups, AChE + neural-like profiles were present along the vasculature and in the trabeculae. AChE + reactivity also was present in lymphoid and reticular cells in the spleen, and in neuronal cell bodies in the superior mesenteric–coeliac ganglion (SM–CG). Neurochemical analysis revealed no significant choline acetyltransferase activity in spleens from control animals. Surgical removal of the SM–CG resulted in a total loss of both noradrenergic (NA) and AChE + nerve profiles, as well as a loss of AChE staining in nonneural compartment in the spleen. On Days 1 and 3 after treatment, chemical sympathectomy with 6-hydroxy-dopamine also resulted in a loss of both NA and AChE nerve profiles in the spleen, except for a few resistant fibers in the hilar region. AChE reactivity in nonneural compartments also was diminished in chemically denervated regions of the spleen. AChE staining in both neural and nonneural profiles progressively increased from 10 to 56 days after chemical sympathectomy, with a time course and distribution pattern similar to NA fibers reinnervating the spleen. AChE + staining was preserved following bilateral vagal nerve transection. The miniscule splenic levels of choline acetyltransferase suggest that at best, only a small density of cholinergic nerves distribute to the rat spleen. Further, what cholinergic innervation is present does not arise from the vagus nerve as suggested in the earlier literature. Collectively, the overlapping distribution of AChE + and NA nerve profiles in spleen and parallel loss of both population of nerve fibers following surgical and chemical sympathectomy support the presence of AChE in NA nerves colocalized with norepinephrine, and thus make AChE + staining an inappropriate marker for cholinergic innervation in the rat spleen.