Synaptic potentiation in the central amygdala involves different mechanisms depending on pain model

Abstract

Negative emotion resulting from nociception is the most serious therapeutic concern especial-ly in treatment of chronic persistent pain. The spino–parabrachio (PB)–amygdaloid pathway originating in the superficial layer of the dorsal horn and terminating in the laterocapsular part (CeLC) of the central amygdala plays a pivotal role in the expression of such pain– related negative emotion (Gauriau and Bernard, 2002). Bird et al. (2005) demonstrated that, in arthritis pain model, the PB–CeLC synaptic potentiation involves protein kinase A–depen-dent enhancement of NMDA receptor function. In contrast, we demonstrated that the PB– CeLC transmission becomes potentiated in rats with neuropathic pain persisting for a week (Ikeda et al., 2007) in a manner not involving NMDA receptor component potentiation, unlike that in the arthritis model rats. To determine whether this difference in the mechanisms of PB–CeLC synaptic potentiation between these pain models results from that in the time– course after operation in these experiments or in the modality of pain in these pain models, we investigated PB–CeLC synaptic potentiation in rats with incipient neuropathic pain. Excitatory postsynaptic currents (EPSC) evoked by PB afferent stimulation in CeLC neurons were evaluated in the brain slices after measurement of allodynic response with von Frey fila-ments in vivo at 6 – 8 hr after the nerve ligation. The allodynic response was observed only in the left–side hindpaw and evoked EPSC amplitude was potentiated in the bilateral CeLCs. This potentiation, observed in both sides of the CeLC, was primarily due to enhanced non– NMDA receptor components, in a manner similar to that observed in the same pain model with prolonged (1 week) period of pain. In conclusion, the different synaptic mechanisms underlying the PB–CeLC synaptic potentiation between arthritis and neuropathic pain models do not result from the difference in their time–course but rather from their distinct spatiotemporal patterns of central activation with distinct modalities.