Norepinephrine release in the amygdala in response to footshock and opioid peptidergic drugs.

These experiments used in vivo microdialysis and high-performance liquid chromatography to examine, in rats, norepinephrine (NE) release in the amygdala induced by footshock and systemic administration of drugs affecting the opioid peptidergic system. A microdialysis probe was inserted into a previously implanted guide cannula aimed at the amygdala and the rat was placed in a box with a stainless-steel grid floor through which a single footshock was delivered. Samples were collected and analyzed at 15-min intervals. Footshock stimulation increased NE levels and the magnitude of the increase varied with footshock intensity. Relative to baseline levels, intensities of 0.3, 0.7 and 1.2 mA (3 s) induced increases of 41, 64 and 97%, respectively. NE levels returned to baseline within 30 min after footshock stimulation. The opioid peptidergic antagonist naloxone (1 mg/kg, i.p.) administered immediately after footshock (0.55 mA for 1 s) potentiated NE release. In contrast, the opioid peptidergic agonist beta-endorphin (10 microgram/kg, i.p.) administered after the footshock blocked the footshock-induced increase in NE levels. The magnitude of NE release was less when the drugs were administered without prior footshock and when the injections were given 30 min after footshock. The findings are consistent with previous evidence that acute, mildly stressful stimulation induces the release of NE in the amygdala as well as with extensive pharmacological evidence indicating that amygdala NE released by arousing stimulation is involved in regulating memory storage and that the opioid peptidergic system influences memory storage by modulating the release of NE in the amygdala.