From: The amygdala between sensation and affect: a role in pain
Pain situation a | Changes in the CeA | Reference |
---|---|---|
Acute somatic stimulations | Changes (mostly excitation) in electrical activity | |
Visceral pain | ||
  ip acetic acid | - Increased c-fos mRNA expression | [24] |
  Esophageal acetic acid | - Increased c-Fos immunoreactivity | [25] |
  Colitis | - Increased neuronal excitability | |
- Enhanced the PB-CeA, but not the BLA-CeA transmission | ||
- Increased crf mRNA expression | ||
  Cystitis | - Increased c-Fos and Krox-24 imunoreactivities | |
- Increased crf mRNA expression | ||
Inflammatory pain | ||
  Intraplantar formalin | - Induced ERK activation in the right CeA | |
  Acid-induced muscle pain | - Increased ERK activation | [32] |
- Enhanced the PB-CeA transmission | ||
  Knee joint arthritis | - Increased spontaneous activity in the right CeA | |
- Increased neuronal excitability in the right CeA | ||
- Enhanced the PB-CeA and the BLA-CeA transmission | ||
- Increased mGluR1 and mGluR5 expression | ||
- Increased phosphorylation of NR1 subunit | ||
Neuropathic pain | ||
  Sciatic nerve ligation or section | - Increased spontaneous and evoked activity differentially in the left and right CeA | |
- Enhanced the PB-CeA transmission | ||
- Increased crf mRNA expression and CRF immunoreactivity | ||
- Increased glucocorticoid receptor mRNA expression | ||
- Increased cell proliferation |