Evidence that cholecystokinin-enhanced retention is mediated by changes in opioid activity in the amygdala.
Mice, partially trained to avoid footshock in a T-maze, showed enhanced retention relative to vehicle-injected mice when treated peripherally with arecoline, D-amphetamine, cholecystokinin octapeptide (CCK-8), epinephrine or naloxone. Both intra-amygdaloid and intraventricular injections of beta-endorphin resulted in amnesia. D-amphetamine and arecoline blocked the amnestic effect of beta-endorphin administered into the amygdala but it required higher doses for CCK-8, epinephrine and naloxone to block the amnestic effect of beta-endorphin. The effects of CCK-8, epinephrine and naloxone showed a differential ability to block amnesia induced by beta-endorphin intraventricularly with epinephrine and naloxone preventing amnesia but CCK-8 not improving retention. This data suggests that the memory enhancement produced by peripherally administered CCK-8 involves the amygdala and that both CCK-8 and epinephrine interact with opioid amnestic mechanisms within the amygdala to alter memory processing.
Flood
J F
JF
VA Medical Center, Geriatric Research Educational and Clinical Center, St. Louis, MO 63106.
Garland
J S
JS
Morley
J E
JE
D000679:Amygdala / Q000378:metabolism*; D000818:Animals; D004723:Endorphins / Q000378:metabolism*; D004837:Epinephrine / Q000494:pharmacology; D007267:Injections; D007276:Injections, Intraventricular; D008297:Male; D008568:Memory / Q000187:drug effects* / Q000502:physiology; D051379:Mice; D008815:Mice, Inbred Strains; D009270:Naloxone / Q000494:pharmacology; D012844:Sincalide / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D001615:beta-Endorphin / Q000494:pharmacology
D004723:Endorphins; D009270:Naloxone; D001615:beta-Endorphin; D012844:Sincalide; D004837:Epinephrine