The capsular part of the central amygdala (CeC) is called the "nociceptive amygdala," as it receives nociceptive information from various pathways, including monosynaptic input from the lateral part of the parabrachial nucleus (LPB), a major target of ascending neurons in the spinal and medullary dorsal horn. LPB-CeC synaptic transmission is mediated by glutamate but the fibers from the LPB also contain calcitonin gene-related peptide (CGRP) and the CeC is rich in CGRP-binding sites. CGRP might be released in response to strong nociception and activate these CGRP receptors. Though it has been shown that CGRP affects the excitatory postsynaptic current (EPSC) amplitude at this synapse in a manner sensitive to NMDA receptor (NMDA-R) blockers, the effect of CGRP on postsynaptic NMDA-R-mediated current recorded in isolation has never been directly examined. Thus, we evaluated the effects of CGRP on NMDA-R-mediated EPSCs that were pharmacologically isolated in brain slices from naive mice. CGRP significantly increased the amplitude of EPSCs mediated by NMDA-Rs in a manner dependent on protein kinase A activation, but not that mediated by alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors, in concentration-dependent and antagonist-sensitive manners. This CGRP-induced potentiation of synaptic NMDA-R function would have a potent impact on the strengthening of the nociception-emotion link in persistent pain.