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THE AF64A MODEL OF CHOLINERGIC HYPOFUNCTION - AN UPDATE

机译：胆碱能功能障碍的AF64A模型-更新

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Based on numerous reports in the literature since 1980, one can now conclude that ethylcholine aziridinium (AF64A) is selective for the cholinergic system in vivo, and that the effect is both dose- and site-dependent. Thus, AF64A treatment, under the correct conditions of dose and time will result in selective reductions in levels of ACh, AChE, ChAT, HAChT, and K+- and ouabain-stimulated release of ACh. While other neurotransmitters may also be affected in brains of AF64A treated rats, the effect is only transient and is most probably secondary to the initial cholinergic deficit induced by AF64A, reflecting an adaptive reaction of these neurotransmitter systems, which are normally integrated with cholinergic interconnections, to the cholinergic deficiency induced by AF64A. This paper provides a historical perspective for the development of AF64A as a selective cholinotoxin, and surveys its potential mechanisms of action at the neurochemical and molecular levels. Moreover, the availability of an animal model such as the AF64A-treated rat, in which the cholinergic system has been compromised selectively for an extended period of time, has allowed investigators to study a wide variety of questions that relate to factors controlling cholinergic function in vivo. Several key illustrations are presented at the end of this paper. [References: 66]
机译：自1980年以来，根据大量文献报道，现在可以得出结论，乙基胆碱叠氮鎓（AF64A）对体内的胆碱能系统具有选择性，其作用是剂量依赖性和位点依赖性的。因此，在正确的剂量和时间条件下进行AF64A治疗将选择性降低ACh，AChE，ChAT，HAChT，K +和哇巴因刺激的ACh释放水平。虽然其他神经递质也可能会在经AF64A治疗的大鼠的大脑中受到影响，但这种作用只是短暂的，最有可能继发于AF64A诱发的初始胆碱能缺乏，这反映了这些神经递质系统的适应性反应，这些系统通常与胆碱能的相互联系整合在一起， AF64A引起的胆碱能缺乏。本文为AF64A作为选择性胆碱毒素的发展提供了历史展望，并调查了其在神经化学和分子水平上的潜在作用机理。此外，动物模型（例如经AF64A处理的大鼠）的有效性，其中胆碱能系统在很长一段时间内受到选择性损害，使研究者能够研究与控制胆碱能功能的因素有关的各种问题。体内。本文末尾提供了几个关键的插图。 [参考：66]

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