Systemic Administration of ACTH or Vasopressin Reverses the Amnestic Effect of Posttraining β-Endorphin or Electroconvulsive Shock but Not That of Intrahippocampal Infusion of Protein Kinase Inhibitors

Abstract

Retrograde amnesia was induced in rats trained in step-down inhibitory avoidance by four different treatments: an ip injection of β-endorphin (1.0 μg kg), an electroconvulsive shock (ECS), an intrahippocampal infusion of the calcium/calmodulin protein kinase II inhibitor, KN62 (0.08 μg/side), given 0 h after training, or an intrahippocampal infusion of the protein kinase A inhibitor, KT5720 (0.5 μg/side), given 3 h after training. Pretest ip injections of ACTH (0.2 μg/kg) or vasopressin (10.0 μg/kg), but not saline, reversed the amnesia caused by β-endorphin and ECS but not that caused by the enzyme inhibitors. This suggests that the amnesia produced by intrahippocampal KN62 and KT5720 administration is stronger than that caused by ECS and β-endorphin, possibly because the former interfere directly with specific steps of the core biochemical chain of events that underlies memory consolidation.