Inhibition of cholinesterase elicits muscarinic receptor-mediated synaptic transmission in the rat adrenal medulla
Inhibition of cholinesterase elicits muscarinic receptor-mediated synaptic transmission in the rat adrenal medulla
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DOI：
10.1016/s1566-0702(03)00129-2
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发表时间：
2003-09-30
影响因子：
2.7
通讯作者：
Sunagawa, K
中科院分区：
文献类型：
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作者：
Akiyama, T;Yamazaki, T;Sunagawa, K
为了确定乙酰胆碱酯酶在体内肾上腺髓质胆碱能突触传递中的作用，我们对麻醉大鼠肾上腺髓质采用透析技术，考察了乙酰胆碱酯酶抑制剂对烟碱受体和毒蕈碱受体对儿茶酚胺释放的影响。外源性乙酰胆碱诱导的肾上腺素释放被阿托品（一种毒蕈碱受体拮抗剂）和六甲索铵（一种烟碱受体拮抗剂）抑制。内源性乙酰胆碱（神经刺激）诱导的肾上腺素释放被六甲铵抑制，而阿托品没有抑制作用。在新斯的明（一种乙酰胆碱酯酶抑制剂）的存在下，外源性和内源性乙酰胆碱诱导的儿茶酚胺释放增强。在这两种情况下，肾上腺素释放均被阿托品和六甲溴铵抑制。在存在叶丝氨酸（另一种乙酰胆碱酯酶抑制剂）的情况下，内源性乙酰胆碱诱导的肾上腺素释放也被阿托品抑制。外源性或内源性乙酰胆碱诱导的去甲肾上腺素释放主要被六甲溴铵抑制，无论新斯的明是否存在或不存在。在大鼠肾上腺髓质中，抑制乙酰胆碱酯酶不仅能增强胆碱能突触传递，还能引发毒蕈碱受体介导的肾上腺素释放突触传递。(C) 2003 Elsevier B.V.版权所有
To determine the role of acetylcholinesterase in cholinergic synaptic transmission in the adrenal medulla in vivo, we applied a dialysis technique to the adrenal medulla of anesthetized rats and examined the effect of acetylcholinesterase inhibitor on the contribution of nicotinic and muscarinic receptors to catecholamine release. Exogenous acetylcholine-induced epinephrine release was inhibited by atropine (a muscarinic receptor antagonist) as well as hexamethonium (a nicotinic receptor antagonist). Endogenous acetylcholine (nerve stimulation)-induced epinephrine release was inhibited by hexamethonium but not atropine. In,the presence of neostigmine (an acetylcholinesterase inhibitor), both exogenous and endogenous acetylcholine-induced catecholamine release was enhanced. In either case, epinephrine release was inhibited by atropine as well as hexamethonium. In the presence of eserine (another acetylcholinesterase inhibitor), endogenous acetylcholine-induced epinephrine release was also inhibited by atropine. Exogenous or endogenous acetylcholine-induced norepinephrine release was primarily inhibited by hexamethonium regardless of whether neostigmine was absent or present. In the rat adrenal medulla, the inhibition of acetylcholinesterase not only enhanced cholinergic synaptic transmission but also elicited muscarinic receptor-mediated synaptic transmission for epinephrine release. (C) 2003 Elsevier B.V. All rights reserved.