Grigson P S, Reilly S, Shimura T, Norgren R
Department of Behavioral Science, College of Medicine, Pennsylvania State University, Hershey 17033, USA.
Behav Neurosci. 1998 Feb;112(1):160-71.
Rats with extensive ibotenic acid lesions centered in the gustatory zone of the pontine parabrachial nucleus (PBN) failed to acquire a conditioned taste aversion (CTA) induced by lithium chloride (LiCl) toxicosis (Experiments 1 and 4). This deficit cannot be explained as an inability to either perceive or process gustatory information because lesioned rats that failed to acquire a CTA readily acquired a conditioned flavor preference (Experiment 2). Similarly, the CTA deficit cannot be attributed to an inability to experience or process visceral input because PBN-lesioned rats that failed to acquire a CTA successfully learned an aversion to a trigeminal stimulus, capsaicin, when paired with LiCl-induced illness (Experiment 3). This pattern of results supports the view that cell bodies within the PBN are essential for the associative processes that govern CTA learning.
以脑桥臂旁核（PBN）味觉区为中心出现广泛鹅膏蕈氨酸损伤的大鼠，无法习得由氯化锂（LiCl）中毒诱导的条件性味觉厌恶（CTA）（实验1和4）。这种缺陷不能解释为无法感知或处理味觉信息，因为未能习得CTA的损伤大鼠很容易习得条件性风味偏好（实验2）。同样，CTA缺陷也不能归因于无法体验或处理内脏输入，因为未能习得CTA的PBN损伤大鼠在与LiCl诱导的疾病配对时，成功地学会了对三叉神经刺激物辣椒素产生厌恶（实验3）。这种结果模式支持了这样一种观点，即PBN内的细胞体对于控制CTA学习的联想过程至关重要。
