Neuropathic pain (NP) often presents with comorbidities, including depression and anxiety. The amygdala is involved in the processing of mood disorders, fear, and the emotional-affective components of pain. Hemispheric lateralization of pain processing in the amygdala has recently been brought to light because, independently of the side of the peripheral injury, the right central nucleus of the amygdala (CeA) showed higher neuronal activity than the left in models of inflammatory pain. Although the CeA has been called the ‘nociceptive amygdala’, because of its high content of nociceptive neurones, little is known about changes in its neuronal function in vivo, under NP conditions. Herein, we quantified CeA spontaneous and evoked activity in rats subjected to spinal nerve ligation (SNL), under isoflurane anaesthesia, following application of mechanical and thermal stimuli to widespread body areas. We found that spontaneous and stimulus-evoked neuronal activity was higher in the left CeA at 2 and 6 days after SNL induction and declined afterwards, whereas activity in the right CeA became dominant at 14 days after surgery, independently of the side of surgery. We also observed that systemic injection of pregabalin, which is widely used in patients with NP, reduced CeA spontaneous and stimulus-evoked neuronal activity. Overall, we observed that peripheral nerve injury produced asymmetric plasticity in ongoing and evoked activity in the left and right CeA. Remarkably, at 14 days after SNL induction, enhanced evoked activity in the right CeA persisted compared to short-term increases in activity in the left CeA. The plasticity found in ongoing and evoked activity was inhibited by pregabalin.