The consequences of exciting or destroying the prelimbic cortex (PrL) or the basolateral amygdala (BLA) remain unclear, including the effects on morphine-induced conditioned taste aversion (CTA) in the conditioning and extinction phases, plasma corticosterone (CORT) levels, and c-Fos/p-ERK expressions in the subareas of the medial prefrontal cortex (i.e., PrL, infralimbic cortex [IL], cingulate cortex 1 [Cg1]), basolateral amygdala (BLA), central amygdala (CeA), hippocampus (i.e., CA1, CA2, CA3, and dentate gyrus [DG]), nucleus accumbens (NAc), lateral hypothalamus (LH), and piriform cortex (PC). During conditioning, excitation of the PrL glutamate neurons via NMDA injections disrupted morphine-induced CTA and decreased plasma CORT levels; moreover, c-Fos and p-ERK expression was hyperactive in the PrL and IL but hypoactive in the Cg1 and BLA. In conditioning, excitation of the BLA glutamate neurons via NMDA injections facilitated morphine-induced CTA and increased plasma CORT levels. The expression of c-Fos and p-ERK was hypoactive in the PrL and IL but hyperactive in the BLA. During extinction, lesion of the PrL glutamate neurons via NMDA injections impaired morphine-induced CTA extinction and enhanced plasma CORT levels. The expression of c-Fos and p-ERK was hypoactive in the PrL and IL but hyperactive in the BLA. In extinction, excitation of the PrL glutamatergic neurons via NMDA injections facilitated morphine-induced CTA extinction and did not affect plasma CORT levels; moreover, the expression of c-Fos and p-ERK was hypoactive in the Cg1, PrL, and IL but hyperactive in the BLA. Altogether, the interaction between the PrL and BLA plays a balancing role in morphine-induced CTA conditioning and extinction. During conditioning, the activity of the PrL correlated negatively with plasma CORT secretions, whereas the activity of the BLA correlated positively with the plasma CORT levels. During extinction, the activity of the PrL correlated negatively with plasma CORT secretions; however, the activity of the BLA may be negatively associated with the plasma CORT levels. The data presented here provide some implications for morphine addiction and dependence.

中文翻译：

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前缘皮层与基底外侧杏仁核之间的相互作用有助于吗啡诱导条件性和绝种中的条件性味觉厌恶。

尚不清楚激发或破坏前肢皮质（PrL）或基底外侧杏仁核（BLA）的后果，包括在适应和消光阶段对吗啡诱导的条件性味觉厌恶（CTA），血浆皮质酮（CORT）水平和c-Fos / p-ERK在内侧前额叶皮层区域（即PrL，下肢皮层[IL]，扣带回皮层1 [Cg1]），基底外侧杏仁核（BLA），中央杏仁核（CeA），海马（即，CA1，CA2，CA3和齿状回[DG]，伏伏核（NAc），下丘脑外侧（LH）和梨状皮层（PC）。在调节过程中，通过NMDA注射激发PrL谷氨酸神经元会破坏吗啡诱导的CTA并降低血浆CORT水平。此外，c-Fos和p-ERK的表达在PrL和IL中活跃，但在Cg1和BLA中活跃。在调节中，通过NMDA注射激发BLA谷氨酸神经元促进了吗啡诱导的CTA和血浆CORT水平的升高。c-Fos和p-ERK的表达在PrL和IL中过低，而在BLA中过高。在灭绝过程中，通过NMDA注射引起的PrL谷氨酸神经元病变损害了吗啡诱导的CTA灭绝，并增强了血浆CORT水平。c-Fos和p-ERK的表达在PrL和IL中过低，而在BLA中过高。在灭绝中，通过NMDA注射激发PrL谷氨酸能神经元促进了吗啡诱导的CTA灭绝，并且不影响血浆CORT水平。此外，c-Fos和p-ERK的表达在Cg1，PrL和IL中活性不足，而在BLA中活性较高。共，PrL和BLA之间的相互作用在吗啡诱导的CTA调节和消光中起平衡作用。在调节过程中，PrL的活性与血浆CORT分泌呈负相关，而BLA的活性与血浆CORT水平呈正相关。在灭绝过程中，PrL的活性与血浆CORT分泌呈负相关。但是，BLA的活性可能与血浆CORT水平呈负相关。本文提供的数据为吗啡成瘾和依赖性提供了一些启示。PrL的活性与血浆CORT分泌呈负相关；但是，BLA的活性可能与血浆CORT水平呈负相关。本文提供的数据为吗啡成瘾和依赖性提供了一些启示。PrL的活性与血浆CORT分泌呈负相关；但是，BLA的活性可能与血浆CORT水平呈负相关。本文提供的数据为吗啡成瘾和依赖性提供了一些启示。