Acute organophosphate (OP) poisoning, particularly by suicide attempts, generates high mortality and morbidity. Few studies have systematically addressed the consequences of acute OP intoxication on cognition and memory of survivors. Preclinical evidence suggests that acute OP-induced effects are associated with inhibiting the brain acetylcholinesterase (AChE) enzyme. The OP triazophos has been used worldwide, although its effects on mnemonic processing are yet to be investigated. Based on the above, the present study investigated whether acute triazophos intoxication interferes with the expression and extinction of contextual fear memory in rats. Hippocampal and amygdalar AChE activity and plasma butyrylcholinesterase (BChE) were measured at the end of the experiment to confirm the cholinergic overstimulation. Independent cohorts of animals intoxicated with triazophos were evaluated in the novel object recognition (NOR) test, a less aversive associative memory task. At the dose of 15 mg/kg, triazophos administered immediately after contextual fear conditioning impaired the extinction but not the expression of freezing behavior. Triazophos poisoning induced no changes in the discrimination index in the NOR test. Triazophos inhibited the AChE activity in a time- and brain region-dependent manner. Our findings suggest that fear memory extinction deficits induced by acute triazophos intoxication are accompanied by hippocampal AChE inhibition. The deficient fear extinction associated with acute OP poisoning may represent a behavioral and biochemical phenotype helpful to study mechanisms of neurotoxicity and treatment approach of OP suicide survivors.

急性有机磷 (OP) 中毒，尤其是自杀企图，会导致高死亡率和发病率。很少有研究系统地解决急性 OP 中毒对幸存者认知和记忆的影响。临床前证据表明，急性 OP 诱导的作用与抑制脑乙酰胆碱酯酶 (AChE) 酶有关。OP 三唑磷已在世界范围内使用，但其对助记处理的影响尚待研究。基于上述，本研究调查急性三唑磷中毒是否会干扰大鼠情境恐惧记忆的表达和消失。在实验结束时测量海马和杏仁核 AChE 活性和血浆丁酰胆碱酯酶 (BChE) 以确认胆碱能过度刺激。在新的物体识别 (NOR) 测试（一种不太厌恶的联想记忆任务）中评估了使用三唑磷中毒的独立动物群。在 15 mg/kg 的剂量下，在情境恐惧条件反射后立即给予三唑磷会损害灭绝，但不会损害冻结行为的表达。三唑磷中毒在 NOR 测试中没有引起鉴别指数的变化。三唑磷以时间和大脑区域依赖性方式抑制 AChE 活性。我们的研究结果表明，由急性三唑磷中毒引起的恐惧记忆消退缺陷伴随着海马 AChE 抑制。与急性 OP 中毒相关的恐惧消退不足可能代表一种行为和生化表型，有助于研究 OP 自杀幸存者的神经毒性机制和治疗方法。