The Journal of Neuroscience, November 16, 2005, ():
Critical Role of Calcitonin Gene-Related Peptide 1 Receptors in the Amygdala in Synaptic Plasticity and Pain Behavior
J. Neurosci. Han et al.
25: 10717
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Proposed mechanisms of pain-related synaptic plasticity in the nociceptive amygdala (CeLC). Increased nociceptive signals in the spino-parabrachio(PB)-amygdaloid pain pathway (Neugebauer et al., 2004) lead to enhanced presynaptic release of glutamate (Glu) through metabotropic glutamate receptor subtypes mGluR1 and mGluR5 (Neugebauer et al., 2003;Li and Neugebauer, 2004a). Glutamate acts postsynaptically to activate N-methyl-D-aspartate (NMDA) receptors, which are “silent” under normal conditions but become functional through receptor phosphorylation (NMDAP) by PKA but not PKC (Bird et al., 2005). Change in NMDA rather than AMPA receptor function contributes to synaptic plasticity and pain responses (Li and Neugebauer, 2004b;Bird et al., 2005) through increased calcium (Ca) influx into the cell. The present study shows CGRP1 is the critical molecule to link pre- and postsynaptic mechanisms of pain-related plasticity in the CeLC. Endogenous CGRP released from the parabrachio(PB)-amygdaloid tract activates postsynaptic CGRP1 receptors coupled to PKA to increase NMDA, but not AMPA, receptor function. CGRP1 receptor activation plays an important role in synaptic plasticity and pain processing in the amygdala and in amygdala-mediated pain behavior.
