PKA and ERK, but not PKC, in the amygdala contribute to pain-related synaptic plasticity and behavior.

摘要: The laterocapsular division of the central nucleus amygdala (CeLC) has emerged as an important site pain-related plasticity and pain modulation. Glutamate neuropeptide receptors in CeLC contribute to synaptic behavioral changes arthritis model, but intracellular signaling pathways remain be determined. This study addressed role PKA, PKC, ERK CeLC. Adult male Sprague-Dawley rats were used all experiments. Whole-cell patch-clamp recordings neurons made brain slices from normal with a kaolin/carrageenan-induced monoarthritis knee (6 h postinduction). Membrane-permeable inhibitors PKA (KT5720, 1 μM; cAMPS-Rp, 10 μM) (U0126, activation inhibited arthritic had no effect on transmission control slices. A PKC inhibitor (GF109203x, inactive structural analogue U0126 (U0124, effect. NMDA receptor-mediated component was by KT5720 or U0126; their combined application additive effects. did not inhibit facilitation forskolin-induced PKA-activation. Administration (100 μM, concentration microdialysis probe) into CeLC, striatum (placement control), audible ultrasonic vocalizations spinal reflexes animals. GF109203x U0124 affect behavior. data suggest that ERK, behavior increasing receptor function through independent pathways.