Chronic pain is often accompanied by anxiety and depression disorders. Amygdala nuclei play important roles in emotional responses, fear, depression, anxiety and pain modulation. The exact mechanism of how amygdala neurons are involved in pain and anxiety is not completely understood. The central nucleus of the amygdala (CeA) contains two major subpopulations of GABAergic neurons that express somatostatin (SOM+) or protein kinase Cδ (PKCδ+). In this study, we found about 70% of pERK-positive neurons colocalized with PKCδ+ neurons in the formalin-induced pain model in mice. Optogenetic activation of PKCδ+ neurons was sufficient to induce mechanical hyperalgesia without changing anxiety-like behavior in naïve mice. Conversely, chemogenetic inhibition of PKCδ+ neurons significantly reduced the mechanical hyperalgesia in the pain model. In contrast, optogenetic inhibition of SOM+ neurons induced mechanical hyperalgesia in naïve mice and increased pERK-positive neurons mainly in PKCδ+ neurons. Optogenetic activation of SOM+ neurons slightly reduced the mechanical hyperalgesia in the pain model but did not change the mechanical sensitivity in naïve mice. Instead, it induced anxiety-like behavior. Our results suggest that the PKCδ+ and SOM+ neurons in CeA exert different functions in regulating pain- and anxiety-like behaviors in mice.
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