Crane Adam L, Feyten Laurence E A, Brusseau Alix J P, Dumaresq Synnott Félixe, Ramnarine Indar W, Ferrari Maud C O, Brown Grant E
School of Mathematical and Natural Sciences, University of Arkansas at Monticello, Monticello, Arkansas, USA.
Department of Biological Sciences, Concordia University, Montreal, Quebec, Canada.
Behav Pharmacol. 2025 Oct 1;36(7):500-508. doi: 10.1097/FBP.0000000000000847. Epub 2025 Aug 15.
The fear of predation is pervasive among vertebrate prey species, being characterized by neurobiological and behavioral changes induced by risk exposure. To understand the acquisition and attenuation of fearful phenotypes, such as dimensions of posttraumatic stress, researchers often use animal models, with prey fishes recently emerging as a nontraditional but promising model. Much is known about fear acquisition in prey fishes such as the Trinidadian guppy, Poecilia reticulata, which inhabit high and low predation sites. Little is known, however, about whether a guppy model shows fear attenuation via therapeutic treatments, such as commonly prescribed anxiolytic drugs, like benzodiazepines. In this study, we used Trinidadian guppies from wild populations to explore the interactive effects of exposure to the anxiolytic drug, diazepam, and exposure to predation risk in the form of injured conspecific cues (i.e. alarm cues) that reliably indicate a predator attack. In Experiment 1, juvenile guppies from both high- and low-predation populations were given a 10-min exposure to diazepam (160 µg/l), resulting in the loss of fear behavior when simultaneously presented with alarm cues. In Experiment 2, we found that a prior 10-min exposure to diazepam (160 µg/l) for adult guppies significantly reduced their subsequent fear behavior toward a separate exposure to alarm cues, revealing that diazepam was having direct effects on guppy cognition rather than simply inactivating the alarm cues via chemical alteration. These anxiolytic effects thus add to the growing support for the predictive validity of prey fishes as animal models for exploring fear attenuation in humans.
对被捕食的恐惧在脊椎动物猎物物种中普遍存在,其特征是由风险暴露引起的神经生物学和行为变化。为了理解恐惧表型的获得和减弱,例如创伤后应激的各个方面,研究人员经常使用动物模型,最近猎物鱼类成为一种非传统但很有前景的模型。对于诸如特立尼达孔雀鱼(Poecilia reticulata)等猎物鱼类的恐惧获得,我们已经了解很多,它们栖息在高捕食风险和低捕食风险的区域。然而,对于孔雀鱼模型是否能通过治疗手段,如常用的抗焦虑药物(如苯二氮䓬类药物)来表现出恐惧减弱,我们却知之甚少。在本研究中,我们使用来自野生种群的特立尼达孔雀鱼,来探究暴露于抗焦虑药物地西泮以及暴露于以受伤同种个体的线索(即警报线索)形式存在的捕食风险之间的交互作用,这些警报线索能可靠地表明有捕食者攻击。在实验1中,来自高捕食风险和低捕食风险种群的幼年孔雀鱼被给予10分钟的地西泮暴露(160μg/l),结果当同时呈现警报线索时,它们的恐惧行为消失了。在实验2中,我们发现成年孔雀鱼事先暴露于10分钟的地西泮(160μg/l)后,其随后对单独呈现的警报线索的恐惧行为显著减少,这表明地西泮对孔雀鱼的认知有直接影响,而不仅仅是通过化学改变使警报线索失活。因此,这些抗焦虑作用进一步支持了猎物鱼类作为探索人类恐惧减弱的动物模型的预测有效性。