Rosen J B, Hitchcock J M, Miserendino M J, Falls W A, Campeau S, Davis M
Yale University School of Medicine, Connecticut Mental Health Center, New Haven 06508.
J Neurosci. 1992 Dec;12(12):4624-33. doi: 10.1523/JNEUROSCI.12-12-04624.1992.
The present study is part of an ongoing series of experiments aimed at delineation of the neural pathways that mediate fear-potentiated startle, a model of conditioned fear in which the acoustic startle reflex is enhanced when elicited in the presence of a light previously paired with shock. A number of cortical areas that might be involved in relaying information about the visual conditioned stimulus (the light) in fear-potentiated startle were investigated. One hundred thirty-five rats were given 10 light-shock pairings on each of 2 consecutive days, and 1-2 d later electrolytic or aspiration lesions in various cortical areas were performed. One week later, the magnitude of fear-potentiated startle was measured. Complete removal of the visual cortex, medial prefrontal cortex, insular cortex, or posterior perirhinal cortex had no significant effect on the magnitude of fear-potentiated startle. Lesions of the frontal cortex attenuated fear-potentiated startle by approximately 50%. However, lesions of the anterior perirhinal cortex completely eliminated fear-potentiated startle. The effective lesions included parts of the cortex both dorsal and ventral to the rhinal sulcus and extended from approximately 1.8 to 3.8 mm posterior to bregma. Lesions slightly more posterior (2.3-4.8 mm posterior to bregma) or lesions that included only the perirhinal cortex dorsal to the rhinal sulcus had no effect. The region of the perirhinal cortex in which lesions blocked fear-potentiated startle projects to the amygdala, and thus may be part of the pathway that relays the visual conditioned stimulus information to the amygdala, a structure that is also critical for fear-potentiated startle. In addition, the present findings are in agreement with numerous studies in primates suggesting that the perirhinal cortex may play a more general role in memory.
本研究是正在进行的一系列实验的一部分，旨在描绘介导恐惧增强型惊吓反应的神经通路，恐惧增强型惊吓反应是一种条件性恐惧模型，在该模型中，当在先前与电击配对的光出现时引发听觉惊吓反射，其会增强。研究了一些可能参与在恐惧增强型惊吓反应中传递有关视觉条件刺激（光）信息的皮质区域。135只大鼠在连续2天中的每一天都接受10次光-电击配对，在1-2天后对各个皮质区域进行电解或损毁。1周后，测量恐惧增强型惊吓反应的幅度。完全切除视觉皮质、内侧前额叶皮质、岛叶皮质或后梨状皮质对恐惧增强型惊吓反应的幅度没有显著影响。额叶皮质的损伤使恐惧增强型惊吓反应减弱了约50%。然而，前梨状皮质的损伤完全消除了恐惧增强型惊吓反应。有效的损伤包括梨状沟背侧和腹侧的部分皮质，从囟门后约1.8至3.8毫米处延伸。稍微更靠后的损伤（囟门后2.3-4.8毫米）或仅包括梨状沟背侧梨状皮质的损伤没有效果。损伤阻断恐惧增强型惊吓反应的梨状皮质区域投射到杏仁核，因此可能是将视觉条件刺激信息传递到杏仁核的通路的一部分，杏仁核对于恐惧增强型惊吓反应也至关重要。此外，本研究结果与灵长类动物的大量研究一致，表明梨状皮质可能在记忆中发挥更普遍的作用。
