Background and purpose: The neurobiological circuits underlying chronic pain states are not fully elucidated, limiting available treatment options. While the central amygdala (CeA) is a key hub for integrating pain and stress signals, the role of dynorphin-expressing neurons within the CeA remains poorly understood. Experimental approach: We investigated the role of the CeA dynorphin-expressing (CeA dyn) neurons in the affective and sensory components of chronic neuropathic pain induced by chronic constriction injury. Using dynorphin-Cre mice, we selectively manipulated CeA dyn neuronal activity through chemogenetic, optogenetic and pharmacological approaches. Behavior was assessed using conditioned place preference, real-time place preference paradigms, and measuring mechanical withdrawal thresholds. Finally, whole-brain clearing and anatomical tracing were used to identify projection targets of CeA dyn neurons. Key results: Chemogenetic inhibition of CeA dyn neurons produced a conditioned place aversion in mice with chronic neuropathic pain but had no effect in sham animals. Conversely, optogenetic activation of CeA dyn neurons induced place preference in neuropathic pain mice, with no effect in sham controls. Importantly, neither manipulation altered mechanical withdrawal thresholds. Pharmacological blockade of KOR signaling abolished the place preference associated with optogenetic activation of CeA dyn neurons in neuropathic pain mice. Notably, KOR antagonism revealed a place preference in sham animals, suggesting that dynorphin signaling from CeA dyn neurons is aversive in the absence of chronic pain. In contrast, inhibition of the entire CeA reduced mechanical withdrawal thresholds in neuropathic pain without producing place preference. Anatomical tracing revealed that CeA dyn neurons project to multiple brain regions implicated in affective and pain-related behaviors. Conclusions and Implications: These findings indicate that CeA dyn neurons selectively regulate the affective, but not sensory, component of neuropathic pain. In this context, dynorphin release from CeA dyn neurons appears to be beneficial by alleviating the affective dimension of the pain experience.