Abstract
Dopamine is known to regulate activity within the central amygdala (CeA), an important region for central pain processing. However, its effects at the cellular level have not been well characterized. We targeted pain-responsive CeA neurons for patch-clamp recordings to examine the cellular and synaptic effects of D1 and D2 agonists. Activation of either D1 or D2 receptors induced inhibitory effects, suggesting dopamine signaling in CeA dampens pain-related activity and could be a target for analgesics.
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Funding Information
  • HHS | NIH | National Institute of Neurological Disorders and Stroke (R01-DK116178)
  • HHS | NIH | National Institute of Neurological Disorders and Stroke (R25-NS090978)
  • American Academy of Neurology (Clinical Research Training Scholarship)

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