Synaptic Plasticity in the Amygdala in a Model of Arthritic Pain: Differential Roles of Metabotropic Glutamate Receptors 1 and 5

Pain has a strong emotional-affective dimension, and the amygdala plays a key role in emotionality. Mechanisms of pain-related changes in the amygdala were studied at the cellular and molecular levels in a model of arthritis pain. The influence of the arthritic condition induced in vivo on synaptic...

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Bibliographic Details
Published in:The Journal of neuroscience 2003-01, Vol.23 (1), p.52-63
Main Authors: Neugebauer, Volker, Li, Weidong, Bird, Gary C, Bhave, Gautam, Gereau, Robert W., IV
Format: Article
Language:English
Subjects:
Amygdala - cytology
Amygdala - physiopathology
Animals
Arthritis, Experimental - metabolism
Arthritis, Experimental - physiopathology
Arthritis, Experimental - psychology
Behavior, Animal
Cell Membrane - physiology
Cells, Cultured
Electric Stimulation
Excitatory Postsynaptic Potentials
Male
Neuronal Plasticity
Neurons - physiology
Pain - metabolism
Pain - physiopathology
Pain - psychology
Patch-Clamp Techniques
Rats
Rats, Sprague-Dawley
Receptor, Metabotropic Glutamate 5
Receptors, Metabotropic Glutamate - agonists
Receptors, Metabotropic Glutamate - antagonists & inhibitors
Receptors, Metabotropic Glutamate - physiology
Synaptic Transmission
Up-Regulation
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Summary:Pain has a strong emotional-affective dimension, and the amygdala plays a key role in emotionality. Mechanisms of pain-related changes in the amygdala were studied at the cellular and molecular levels in a model of arthritis pain. The influence of the arthritic condition induced in vivo on synaptic transmission and group I metabotropic glutamate receptor (mGluR1 and mGluR5) function was examined in vitro using whole-cell voltage-clamp recordings of neurons in the central nucleus of the amygdala (CeA). G-protein-coupled mGluRs are implicated in various forms of neuroplasticity as well as in neurological and psychiatric disorders. Synaptic transmission was evoked by electrical stimulation of afferents from the basolateral amygdala (BLA) and the pontine parabrachial (PB) area in brain slices from control (untreated or saline-injected) rats and from arthritic rats. This study shows enhanced synaptic transmission of nociceptive-specific inputs (PB-->CeA synapse) and polymodal sensory inputs (BLA-->CeA synapse) in the arthritis model. CeA neurons from arthritic rats also developed increased excitability compared with control CeA neurons. Synaptic plasticity in the CeA was accompanied by increased presynaptic mGluR1 function and upregulation of mGluR1 and mGluR5. A selective mGluR1 antagonist reduced transmission in CeA neurons from arthritic animals but not in control neurons, and increased levels of mGluR1 and mGluR5 protein were measured in the CeA of arthritic rats compared with controls. Our results show that plastic changes in the amygdala in an arthritis model that produces prolonged pain involve a critical switch of presynaptic mGluR1 expression and function.
ISSN:0270-6474
1529-2401
1529-2401
DOI:10.1523/jneurosci.23-01-00052.2003