Lateral parabrachial nucleus lesions in the rat: Neophobia and conditioned taste aversion

Lateral parabrachial nucleus lesions in the rat: Neophobia and conditioned taste aversion
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DOI:
10.1016/s0361-9230(01)00517-2
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发表时间:
2001-06-01
影响因子:
3.8
通讯作者:
Trifunovic, R
Trifunovic, R
中科院分区:
医学3区
文献类型:
--
作者:
Reilly, S;Trifunovic, R

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本研究探讨的假设,条件性味觉厌恶(CTA)的赤字随之而来的外侧臂旁核(LPBN)的病变可能是由于新恐惧症的中断。在实验1中,受试者进行了测试与三个味觉刺激(丙氨酸,糖精,奎宁)和两个非味觉刺激(辣椒素和杏仁气味)之一。鹅膏蕈氨酸病变的LPBN消除neophobia丙氨酸和糖精,但对neophobia反应奎宁,辣椒素,或杏仁气味没有影响。在实验2中,所有LPBN损伤(LPBNX)大鼠未能开发CTA。这些结果不支持实验假设。损伤引起的对新恐惧症的破坏不仅限于味觉刺激,而且在这一类中,这种缺陷是选择性的。已知LPBNX大鼠不能获得对辣椒素以及丙氨酸的条件性厌恶。因此,在LPBNX大鼠中不存在条件性摄食厌恶并不取决于对目标刺激不存在新恐惧反应。目前的研究结果,虽然暴露了刺激选择性干扰的neophobia,这表明,这种赤字是独立的,而不是负责,没有条件性摄食厌恶LPBN病变的大鼠。(C)2001 Elsevier Science Inc.
The present study investigated the hypothesis that the conditioned taste aversion (CTA) deficit consequent to lesions of the lateral parabrachial nucleus (LPBN) may be due to a disruption of neophobia. In Experiment 1, subjects were tested with one of three taste stimuli (alanine, saccharin, or quinine) and two nontaste stimuli (capsaicin and almond odor). Ibotenic acid lesions of the LPBN eliminated neophobia to alanine and saccharin but had no influence on the neophobic response to quinine, capsaicin, or almond odor. In Experiment 2, all the LPBN-lesioned (LPBNX) rats failed to develop a CTA. These results do not support the experimental hypothesis. Not only was the lesion-induced disruption of neophobia restricted to taste stimuli, the deficit was selective within that category. It is already known that LPBNX rats are unable to acquire conditioned aversions to capsaicin as well as alanine. Thus, the absence of a conditioned ingestional aversion in LPBNX rats is not predicated upon the absence of a neophobic response to the target stimulus. The present results, although exposing a stimulus selective disruption of neophobia, suggest that this deficit is independent of, rather than responsible for, the absence of conditioned ingestional aversions in rats with LPBN lesions. (C) 2001 Elsevier Science Inc.