title: Enhanced group III mGluR-mediated inhibition of pain-related synaptic plasticity in the amygdala.
abstract: 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.
authors.affiliation: Department of Anatomy and Neurosciences and Marine Biomedical Institute, The University of Texas Medical Branch, 301 University Boulevard, Galveston, TX 77555-1069, USA.
authors.forename: Jeong S
authors.initials: JS
authors.lastname: Han
authors.forename: Gary C
authors.initials: GC
authors.lastname: Bird
authors.forename: Volker
authors.initials: V
authors.lastname: Neugebauer
mesh_terms: D000679:Amygdala / Q000187:drug effects / Q000502:physiology*; D000818:Animals; D001169:Arthritis, Experimental / Q000139:chemically induced / Q000503:physiopathology; D004305:Dose-Response Relationship, Drug; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D066298:In Vitro Techniques; D008297:Male; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology; D009473:Neuronal Plasticity / Q000187:drug effects / Q000502:physiology*; D010146:Pain / Q000503:physiopathology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D018094:Receptors, Metabotropic Glutamate / Q000037:antagonists & inhibitors / Q000502:physiology*; D013569:Synapses / Q000187:drug effects / Q000502:physiology*; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology
chemical_list: D018691:Excitatory Amino Acid Antagonists; D018094:Receptors, Metabotropic Glutamate; C102718:metabotropic glutamate receptor 3