Bellgowan P S, Helmstetter F J
Department of Psychology, University of Wisconsin-Milwaukee 53201, USA.
Behav Neurosci. 1996 Aug;110(4):727-36. doi: 10.1037//0735-7044.110.4.727.
A single brief exposure to moderately intense while noise is sufficient to produce opioid-mediated antinociception in rats. This form of stress-induced hypoalgesia represents a response to unconditional fear or anxiety. Three experiments compared the neural circuits responsible for learned versus unlearned fear responses. Male rats received lesions of the medial geniculate nucleus, lateral or central nuclei of the amygdala, or the ventral, dorsal lateral, or dorsal medial periaqueductal gray (PAG). Controls showed a pronounced elevation in tail-flick latency following presentation of 90-dB white noise. All lesions, with the exception of dorsolateral and dorsomedial PAG, significantly blocked this response. These results support the idea that hypoalgesia produced by aversive auditory stimuli uses a common neural circuit regardless of whether the response is a product of associative learning or unconditional fear/anxiety.
对大鼠单次短暂暴露于中等强度白噪声足以产生阿片类药物介导的抗伤害感受。这种应激诱导的痛觉减退形式代表了对无条件恐惧或焦虑的一种反应。三项实验比较了负责习得性与非习得性恐惧反应的神经回路。雄性大鼠接受内侧膝状体核、杏仁核外侧或中央核、或腹侧、背外侧或背内侧导水管周围灰质（PAG）的损伤。对照组在呈现90分贝白噪声后，甩尾潜伏期显著延长。除背外侧和背内侧PAG外，所有损伤均显著阻断了这种反应。这些结果支持了这样一种观点，即厌恶听觉刺激产生的痛觉减退使用了共同的神经回路，无论该反应是联想学习的产物还是无条件恐惧/焦虑的结果。
