Anti-nociception following exposure to trimethylthiazoline, peripheral or intra-amygdala estrogen and/or progesterone.

Estradiol (E(2)) and/or progesterone (P) to the amygdala may influence stress-induced analgesia following predator odor, trimethylthiazoline (TMT), exposure. Ovariectomized (ovx) rats were administered subcutaneous (SC) or intra-amygdala vehicle, E(2), P, or E(2)+P. The effects on performance in a test of pain sensitivity, the tailflick task, was observed in animals that experienced an acute exposure to TMT or no odor (control) in a small chamber. Rats that were exposed to TMT had increased tailflick latencies compared to rats not exposed to TMT, this was partially attenuated by the opiate antagonist naloxone. Systemic E(2), P, or E(2)+P increased tailflick latencies compared to vehicle administration to ovx rats. Ovx rats administered E(2)+P to the amygdala had increased tailflick latencies compared to control rats. These data suggest that following exposure to predator odor, pain sensitivity in the tailflick task is decreased and that E(2) and/or P may have actions in the amygdala to produce similar anti-nociceptive effects.