Spector A C, Scalera G, Grill H J, Norgren R
Department of Psychology, University of Florida, Gainesville 32611-2250, USA.
Behav Neurosci. 1995 Oct;109(5):939-54.
Rats with either electrolytic (Experiment 1) or excitotoxic lesions (Experiment 2) that had been electrophysiologically centered in the gustatory zone of the parabrachial nuclei (PBN) were tested for sucrose and NaCl taste detection thresholds in a conditioned avoidance task. With 1 exception, all of these rats had previously shown severe deficits in acquiring an LiCl-based conditioned taste aversion (CTA) to sucrose, NaCl, or alanine. The rats with excitotoxic lesions also had failed to express a depletion-induced sodium appetite. Despite the uniformity of these deficits, the rats with lesions exhibited varied performance in the detectability task. Roughly 1/3 of the rats did not perform competently, 1/3 had elevated thresholds, and 1/3 showed no or only marginal impairments in taste detectability. These findings demonstrate that the elimination of CTA following PBN lesions is not necessarily linked to an impairment in taste signal detection. Thus, PBN-induced deficits on 1 taste-related task do not entirely correspond with impairments on another.
对那些通过电解法(实验1)或兴奋性毒性损伤法(实验2)损毁脑桥臂旁核(PBN)味觉区且已在电生理上定位准确的大鼠,在条件性回避任务中测试其蔗糖和氯化钠味觉检测阈值。除1只大鼠外,所有这些大鼠此前在获得基于氯化锂的对蔗糖、氯化钠或丙氨酸的条件性味觉厌恶(CTA)方面均表现出严重缺陷。患有兴奋性毒性损伤的大鼠也未能表现出因缺乏钠而引起的摄钠欲望。尽管这些缺陷具有一致性,但有损伤的大鼠在可检测性任务中的表现各不相同。大约1/3的大鼠表现不佳,1/3的大鼠阈值升高,1/3的大鼠在味觉可检测性方面未表现出损伤或仅有轻微损伤。这些发现表明,PBN损伤后CTA的消除不一定与味觉信号检测受损有关。因此;PBN引起的一项味觉相关任务的缺陷并不完全与另一项任务的损伤相对应。