Identification of the opioid receptors involved in passive-avoidance learning in the day-old chick during the second wave of neuronal activity

Long-term memory formation for passive-avoidance learning in the day-old chick is known to have two distinct time windows of protein synthesis (F.M. Freeman, S.P.R. Rose, A.B. Scholey, 1995. Two time windows of anisomycin-induced amnesia for passive-avoidance training in the day-old chick. Neurobiol. Learn. Mem. 63, 291-295). The lobus parolfactorius (LPO) is thought to be an important site for the second wave of protein synthesis which occurs 4-5 h after training. Birds received bilateral intracranial injections of agonists and antagonists for the μ-, δ-, κ-opioid receptors and the opioid receptor-like (ORL₁) receptor directly into the LPO at 5 h post-training and were tested for recall 24 h later. Also, 100 μM β-funaltrexamine (β-FAN), a μ-opioid receptor antagonist, significantly impaired memory formation (P<0.01). The δ-opioid receptor was also involved in memory formation at this time-point since antagonism of this receptor by 1 mM ICI-174,864 caused amnesia (P<0.01) which was reversed by the agonist, DPLPE. The κ-opioid receptor appeared not to be involved during the second phase of neuronal activity since neither stimulation by dynorphin nor inhibition by nor-BIN caused amnesia for the task. The ORL₁ receptor agonist orphanin FQ also had no effect suggesting that this receptor was not involved at this 5-h time-point. Cytosolic and mitochondrial protein synthesis has been shown to be important in passive-avoidance learning in the day-old chick. Both chloramphenicol (CAP) and anisomycin (ANI), inhibitors of mitochondrial and cytosolic protein synthesis, respectively, caused disruption when injected 5 h post-training into the LPO (P<0.05). Endomorphin-2 (Endo-2), a μ-opioid receptor agonist, reversed both the ANI- and CAP-sensitivity. However, DPLPE, a δ-opioid receptor agonist, only reversed the effect due to CAP. Possible mechanisms for these effects are discussed. Copyright (C) 2000 Elsevier Science B.V.