Enhanced group III mGluR-mediated inhibition of pain-related synaptic plasticity in the amygdala.

Pain has a strong emotional component. A key player in emotionality, the amygdala is also involved in pain processing. Our previous studies showed synaptic plasticity in the central nucleus of the amygdala (CeA) in a model of arthritic pain. Here, we address the role of group III metabotropic glutamate receptors (mGluRs) in the regulation of synaptic transmission in CeA neurons. Whole-cell current- and voltage-clamp recordings were made from neurons in the latero-capsular part of the CeA in brain slices from control rats and arthritic rats (>6 h postinduction). The latero-capsular part of the CeA is the target of the spino-parabrachio-amygdaloid pain pathway and is now designated as the "nociceptive amygdala". Monosynaptic excitatory postsynaptic currents (EPSCs) were evoked by electrical stimulation of afferents from the pontine parabrachial (PB) area. LAP4 decreased the amplitude of EPSCs more potently in CeA neurons from arthritic rats (EC(50)=1.2 nM) than in control animals (EC(50)=11.5 nM). The inhibitory effect of LAP4 was reversed by a selective group III mGluR antagonist (UBP1112). During the application of LAP4, paired-pulse facilitation was increased, while no significant changes in slope conductance and action potential firing rate of CeA neurons were observed. These data suggest that presynaptic group III mGluRs are involved in the regulation of synaptic plasticity in the amygdala in an arthritis pain model.