Arthurs Joe, Lin Jian-You, Reilly Steve
University of Illinois at Chicago, Department of Psychology, United States.
University of Illinois at Chicago, Department of Psychology, United States.
Neurobiol Learn Mem. 2018 Dec;156:24-32. doi: 10.1016/j.nlm.2018.10.004. Epub 2018 Oct 15.
Taste neophobia is a feeding system defense mechanism that limits consumption of an unknown, and therefore potentially dangerous, edible until the post-ingestive consequences are experienced. We found that transient pharmacological inhibition (induced with the GABA agonists baclofen and muscimol) of the gustatory thalamus (GT; Experiment 1), but not medial amygdala (MeA; Experiment 2), during exposure to a novel saccharin solution attenuated taste neophobia. In Experiment 3 we found that inhibition of MeA neurons (induced with the chemogenetic receptor hM4DGi) enhanced the expression of taste neophobia whereas excitation of MeA neurons (with hM3DGq) had no influence of taste neophobia. Overall, these results refine the temporal involvement of the GT in the occurrence of taste neophobia and support the hypothesis that neuronal excitation in the GT is necessary for taste neophobia. Conversely, we show that chemogenetically, but not pharmacologically, inhibiting MeA neurons is sufficient to exaggerate the expression of taste neophobia.
味觉新恐惧症是一种进食系统防御机制，它会限制对未知且因此可能有危险的可食用物质的摄入，直到体验到摄入后的后果。我们发现，在接触新型糖精溶液期间，味觉丘脑（GT；实验1）而非内侧杏仁核（MeA；实验2）的短暂药理学抑制（由GABA激动剂巴氯芬和蝇蕈醇诱导）可减轻味觉新恐惧症。在实验3中，我们发现抑制MeA神经元（由化学遗传受体hM4DGi诱导）会增强味觉新恐惧症的表现，而兴奋MeA神经元（用hM3DGq）对味觉新恐惧症没有影响。总体而言，这些结果细化了GT在味觉新恐惧症发生中的时间参与情况，并支持了这样的假设，即GT中的神经元兴奋对于味觉新恐惧症是必要的。相反，我们表明，通过化学遗传学而非药理学方法抑制MeA神经元足以夸大味觉新恐惧症的表现。
