Acetylcholinesterase (AChE) inhibitors modulate acetylcholine hydrolysis and hence play a key role in determining the cholinergic tone and in implementing its impact on the cholinergic blockade of inflammatory processes. Such inhibitors may include rapidly acting small molecule AChE-blocking drugs and poisonous anti-AChE insecticides or war agent inhibitors which penetrate both body and brain. Notably, traumatized patients may be hyper-sensitized to anti-AChEs due to their impaired cholinergic tone, higher levels of circulation pro-inflammatory cytokines and exacerbated peripheral inflammatory responses. Those largely depend on the innate-immune system yet reach the brain via vagus pathways and/or disrupted blood-brain-barrier. Other regulators of the neuro-inflammatory cascade are AChE-targeted microRNAs (miRs) and synthetic chemically protected oligonucleotide blockers thereof, whose size prevents direct brain penetrance. Nevertheless, these larger molecules may exert parallel albeit slower inflammatory regulating effects on brain and body tissues. Additionally, oligonucleotide aptamers interacting with innate immune Toll-Like Receptors (TLRs) may control inflammation through diverse routes and in different rates. Such aptamers may compete with the action of both small molecule inhibitors and AChE-inhibiting miRs in peripheral tissues including muscle and intestine. However, rapid adaptation processes, visualized in neuromuscular junctions enable murine survival under otherwise lethal anti-cholinesterase exposure; and both miR inhibitors and TLR-modulating aptamers may exert body-brain signals protecting experimental mice from acute inflammation. The complex variety of AChE inhibiting molecules identifies diverse body-brain communication pathways which may rapidly induce long-lasting central reactions to peripheral stressful and inflammatory insults in both mice and men.

乙酰胆碱酯酶（AChE）抑制剂可调节乙酰胆碱的水解，因此在确定胆碱能调和实现其对炎症过程的胆碱能阻滞的作用中起关键作用。这类抑制剂可包括能迅速渗透小分子AChE的药物和有毒的抗AChE杀虫剂或渗透到人体和大脑的战争抑制剂。值得注意的是，受创伤的患者由于其胆碱能减弱，循环促炎细胞因子水平升高和外周炎症反应加重，可能会对抗AChE过敏。这些主要依靠先天免疫系统，但通过迷走途径和/或破坏的血脑屏障到达大脑。神经炎性级联反应的其他调节剂是靶向AChE的microRNA（miR）及其合成化学保护的寡核苷酸阻滞剂，其大小可防止直接的大脑渗透。尽管如此，这些较大的分子可能会发挥平行作用，尽管对大脑和身体组织的炎症调节作用较慢。另外，与先天免疫Toll样受体（TLR）相互作用的寡核苷酸适体可以通过多种途径和不同速率控制炎症。这样的适体可以与包括肌肉和肠的外周组织中的小分子抑制剂和抑制AChE的miR两者的作用竞争。然而，在神经肌肉接头中观察到的快速适应过程可使鼠在其他致命的抗胆碱酯酶暴露下存活。miR抑制剂和TLR调节适体都可能产生人脑信号，从而保护实验小鼠免于急性炎症。多种复杂的AChE抑制分子可识别多种人体与大脑的通讯途径，这些途径可迅速诱发对小鼠和男性外周应激和炎性损伤的持久中枢反应。