經常經歷壓力事件會增加罹患焦慮症與憂鬱症的風險；然而此一風險卻存在著相當大的個體差異。在動物的焦慮症模式研究，也發現類似的個體差異現象。造成個體對壓力差異反應之生理相關影響因子，以及主要調控的神經網絡並不清楚。 在本研究中，我們利用長期的社交挫敗壓力和社會交往試驗，將C57BL/6小鼠依壓力敏感反應和壓力耐受反應分成「敏感性」和「耐受性」二組。此二組在聽覺恐懼制約模式中，呈現不同程度的制約恐懼反應，但是其先天的焦慮和憂鬱行為反應，並沒有差異。敏感性小鼠在經歷恐懼制約後，其杏仁體基底側核（basal lateral amygdala）的神經元，表現c-Fos蛋白的數目與腦內衍生神經滋養因子蛋白的表達量，比耐受性組高。利用腦內衍生神經滋養因子基因剔除的策略，我們發現恐懼制約訓練所誘發增加的杏仁體基底側核腦內衍生神經滋養因子，為決定制約恐懼反應程度的重要因子。此外，耐受性小鼠對恐懼制約所導致的心血管和皮質酮反應，則有較快恢復的能力。全身性地給予耐受性小鼠正腎上腺素再攝取抑制劑(norepinephrine reuptake inhibitor) atomoxetine，會增加恐懼制約後杏仁體基底側核神經元表現c-fos蛋白的數目，並加強其恐懼反應。相反地，β腎上腺素接受體拮抗劑(β-adrenergic receptor antagonist) propranolol會減少敏感性小鼠因恐懼制約訓練所誘發杏仁體基底側核神經元表現c-fos蛋白的數目，並降低恐懼反應。 最後，我們以雙側光遺傳學調控和神經迴路逆行追踪技術，證明腦前額葉皮質層（prefrontal cortex）神經元，控制杏仁體基底側核神經細胞活化的程度、調控杏仁體基底側核釋放腦內衍生神經滋養因子的量、以及調節制約恐懼反應的程度。 總結本研究，我們認為恐懼制約刺激所誘導的個體差異現象，與個體杏仁體基底側核所釋放腦內衍生神經滋養因子的量不同有關。而腦前額葉皮質層神經元投射至到杏仁體基底側核的神經路徑，則對恐懼制約的感受度扮演重要的調控角色。

Experiencing stressful life events increase the risk of later developing anxiety and depressive disorders. While everyone experiences their stressful events, there is considerable heterogeneity in responses. Fear conditioning in animals has been used extensively to model clinical anxiety disorders. Each individual exhibits marked differences in their propensity to undergo fear conditioning, the physiologically relevant mediators and neuronal network have not yet been fully characterized. In the present study, we grouped the stress-resistant and stress-susceptible C57BL/6 inbred mice by chronic social defeat stress (CSDS) and social interaction test (SIT) paradigms. They display different levels of fear responses in an auditory fear conditioning paradigm, while there were no significant differences between groups in innate anxiety- and depressive-like behaviors. Susceptible mice had significantly more c-Fos protein expression in neurons of the basolateral amygdala (BLA) after experiencing the conditioning. Through the use of conditional brain-derived neurotrophic factor (BDNF) knockout strategies, we find that elevated BLA BDNF level following fear conditioning training is a key mediator contributing to determine the levels of conditioned fear responses. Results also show that relative to susceptible mice, resistant mice had a much faster recovery from conditioned stimuli-induced cardiovascular and corticosterone responses. Systemic administration of norepinephrine reuptake inhibitor atomoxetine increased c-Fos protein expression in BLA neurons following fear conditioning training and promoted the expression of conditioned fear in resistant mice. Conversely, administration of β-adrenergic receptor antagonist propranolol reduced fear conditioning training-induced c-Fos protein expression in BLA neurons and reduced conditioned fear responses in susceptible mice. Furthermore, by using bidirectional optogenetic manipulations and retrograde tract-tracing technique, we demonstrate that the degree of prefrontal cortex (PFC) projection control of BLA activity modulates the levels of conditioned fear responses via regulating BDNF released from BLA. In conclusion, the data establish that naturally occurring differences in conditioned stimuli-induced BDNF release from the BLA functionally mediate individual differences in the acquisition and expression of conditioned fear, and that PFC inputs to the BLA uniquely regulate the susceptibility to fear conditioning.

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