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The Journal of Neuroscience, January 1, 2003, 23(1):52-63
Synaptic Plasticity in the Amygdala in a Model of Arthritic Pain:
Differential Roles of Metabotropic Glutamate Receptors 1 and 5
Volker
Neugebauer1,
Weidong
Li1,
Gary C.
Bird1,
Gautam
Bhave2, and
Robert W.
Gereau IV2
1 Department of Anatomy and Neurosciences and Marine
Biomedical Institute, The University of Texas Medical Branch,
Galveston, Texas 77555-1069, and 2 Division of
Neuroscience, Baylor College of Medicine, Houston, Texas 77030
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 (BLACeA 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.
Key words:
amygdala; arthritis pain; electrophysiology; metabotropic glutamate receptors; nociception; patch-clamp; plasticity; synaptic transmission
Copyright © 2003 Society for Neuroscience 0270-6474/03/23152-12$05.00/0
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