Compensatory Neural Circuits for Learning Fear Without the BasolateralAmygdala.

Pavlovian Fear Conditioning;Central Amygdala;Basolateral Amygdala;Rat;Glutamate;Fear;Science (General);Science;Neuroscience

Zimmerman, Joshua M.Sutton, Michael Mark ;

University of Michigan

关键词: Pavlovian Fear Conditioning;    Central Amygdala;    Basolateral Amygdala;    Rat;    Glutamate;    Fear;    Science (General);    Science;    Neuroscience;   

Others  :  https://deepblue.lib.umich.edu/bitstream/handle/2027.42/77739/joshuamz_1.pdf?sequence=1&isAllowed=y

瑞士|英语

来源: The Illinois Digital Environment for Access to Learning and Scholarship

【 摘 要 】

This dissertation explores the neural circuitry necessary to compensate for the acquisition and expression of Pavlovian conditioned fear in the absence of the basolateral amygdala. Historically, the basolateral amygdala is viewed as essential for conditioned fear. However, the recent discovery that rats can acquire conditioned fear without the basolateral amygdala through overtraining, suggests another structure can compensate for this loss.In exploring the ability of the central amygdala to compensate for the loss of the basolateral amygdala, it is shown that in rats with pre-training basolateral amygdala lesions, conditioned fear can be acquired after overtraining. Furthermore, lesions or temporary inactivation of the central amygdala completely block the ability of rats to acquire and express conditioned fear, even in rats with an intact basolateral amygdala. This suggests that the central amygdala is critical for the acquisition and expression of conditioned fear even in rats with an intact basolateral amygdala.The bed nucleus of the stria terminals has similar neuroanatomical connectivity to the amygdala suggesting that the bed nucleus might mediate the expression of conditioned fear in the absence of the basolateral amygdala. This possibility is explored using post-training lesions and pre-training temporary inactivation of the bed nucleus in rats with basolateral amygdala lesions. While lesions and temporary inactivation of the bed nucleus blocked the expression of contextual fear, they had no effect on cued fear, suggesting that the bed nucleus is not the locus of compensation for conditioned fear in the absence of the basolateral amygdala.Acknowledging that the central amygdala is critical for the acquisition of fear, the possibility that the central nucleus is also involved in the extinction of conditioned fear was examined. It was found that AMPA receptor antagonism in either nucleus blocks the expression of conditioned fear but has no effect on extinction. Alternatively, NMDA receptor antagonism in the basolateral, but not central amygdala, blocks extinction, suggesting that NMDA receptor dependent plasticity within the central amygdala is not necessary for the extinction of conditioned fear. In conclusion, this dissertation demonstrates discrete roles for the central and basolateral amygdala in the acquisition and extinction of conditioned fear, respectively.