The lateral parabrachial nucleus (LPB) collects nociceptive information from the spinal cord and trigeminal sensory system and sends it to the central nucleus of the amygdala (CeA). This LPB-CeA pathway undergoes extensive synaptic plasticity in various rodent models of persistent pain and plays an essential role in “nociplastic” expression of widespread sensitization (Miyazawa et al, 2018; Sugimoto et al, 2021). However, as this pathway also transmits signals other than nociception, it remains elusive whether the plastic changes at LPB-CeA synapses are specific to pain-associated neuron pairs. We selectively activated synaptic transmission between pain-associated pairs of LPB and CeA neurons using the FosTRAP technique, in which channelrhodopsin-2 (ChR2) and td-Tomato were expressed in LPB neurons and CeA neurons, respectively, following persistent inflammatory pain to activate c-Fos expression in these regions. In brain slices from the FosTRAP mice, we recorded light-evoked excitatory postsynaptic currents (leEPSCs) from “FosTRAPed” CeA neurons and found 1) leEPSC amplitude was larger specifically in these pairs and 2) a second-shot stimulation given 4-8 weeks after the first one resulted in larger leEPSC amplitude in these pairs, which was, unexpectedly, observed in animals also with non-inflammatory brief stimulation. These results suggest that the LPB-CeA synaptic potentiation occurs specifically between pain-associated pairs, which would be primed for plastic changes in response to future aversive events of various types.