Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Enhanced group III mGluR-mediated inhibition of pain-related synaptic plasticity in the amygdala. 1508 88

Metabotropic glutamate receptors (mGluRs) play important roles in neuroplasticity and disorders such as persistent pain. Group I mGluRs contribute to pain-related sensitization and synaptic plasticity of neurons in the laterocapsular division of the central nucleus of the amygdala (CeLC), although the roles of groups II and III mGluRs are not known. Extracellular single-unit recordings were made from 60 CeLC neurons in anesthetized adult rats. Background activity and evoked responses were measured before and during the development of the kaolin/carrageenan-induced knee-joint arthritis. Drugs were administered into the CeLC by microdialysis before and/or after arthritis induction. A selective group III mGluR agonist (LAP4) inhibited CeLC neurons' responses to stimulation of the knee and ankle in arthritis (n = 7) more potently than under normal conditions (n = 14). A selective group II agonist (LY354740) inhibited responses under normal conditions (n = 12) and became more potent in inhibiting responses to noxious stimulation of the knee in arthritis (n = 10). The effect of LY354740 on innocuous stimulation of the knee and stimulation of the ankle did not change in arthritis. Antagonists for groups II (EGLU, n = 9) and III (UBP1112, n = 8) had no effects under normal conditions. In arthritis, UPB1112 (n = 5) facilitated the responses to stimulation of knee and ankle, whereas EGLU (n = 5) selectively increased the responses to stimulation of the knee. These data suggest that mGluRs of groups II and III can inhibit nociceptive processing in CeLC neurons. The increased function and endogenous activation of group II mGluRs in the arthritis pain model appear more input-selective than the general changes of group III mGluRs.
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PMID:Differential changes of group II and group III mGluR function in central amygdala neurons in a model of arthritic pain. 1676 Mar 43