Naloxone attenuates amnesia caused by amygdaloid stimulation: the involvement of a central opioid system.

This study investigated the effect of naloxone on amnesia produced by subseizure amygdaloid stimulation. Animals were trained in an inhibitory avoidance task, and given amygdaloid stimulation following training. Immediately after training, prior to stimulation, naloxone was injected either peripherally (i.p.) or into the bed nucleus of the stria terminalis (BNST) where the Met-enkephalin-containing fibers from the amygdala terminate. Amygdaloid stimulation caused retention deficits. The deficits were attenuated by 3.0 mg/kg naloxone given peripherally or by 1.0 microgram or 0.3 microgram naloxone injected bilaterally into the BNST. The attenuative effect was anatomically and receptor specific: 0.3 microgram of naloxone injected into the caudate nucleus was ineffective; the attenuative effect of naloxone was antagonized by simultaneous injection of 1.5 or 4.5 micrograms levorphanol into the BNST. These results suggest that endogenous opioids, possibly the enkephalins of the stria terminalis released into the BNST following amygdaloid stimulation, are at least partially involved in mediating the effect of amygdaloid stimulation on memory.