The excitatory transmission from the solitary tract (TS) primary afferents to the second-order neurons in the nucleus of the solitary tract (NTS) depends largely on the energetic supply through monocarboxylate transporters (MCTs) (Nagase et al., 2014). We examined whether this large dependency of the excitatory transmission on lactate supply observed in the TS-NTS synapse is commonly shared by brain circuits underlying pain as "sensory and emotional experience". The lateral parabrachial nucleus (LPB) is the site where the nociceptive information arising from the spinal dorsal horn and trigeminal nerve converges and functions as a relay of these signals to the pain-associated networks. The central amygdala (CeA) is the most important target of the ascending LPB projections, which undergoes robust synaptic potentiation in various pain models (Kato et al., 2018). In brain slices prepared from rats and mice, the excitatory synaptic transmission from the LPB to the CeA was significantly attenuated by inhibition of MCTs with 4-hydroxycinnamic acid (4-CIN) without significant changes in paired-pulse ratio. This effect was similarly observed in setups where LPB fibers were stimulated electrically and optogenetically. Interestingly, in the current clamp recordings, blockade of MCTs resulted in postsynaptic depolarization in the CeA neurons, unlike in the pyramidal neurons in the lateral amygdala, hippocampal CA1 and Purkinje neurons in the cerebellum, which were hyperpolarized by activation of K_ATP channels. As the excitability of CeA neurons is a crucial determinant of the emotional/aversive aspects of pain, the pharmacological regulation of the lactate transport in the CeA would be a candidate as a target for resetting aberrantly augmented nociception-emotion link and malfunctioning descending regulation.