Participation of Opioid System in Acquisition of Prenatal Ethanol-related Memories: effects upon neonatal and infantile responsiveness to the drug

MIRANDA MORALES RS; MOLINA JC; SPEAR NE; ABATE P

SAN DIEGO, CA, USA

Congreso; 32nd Scientific Meeting of the Research Society on Alcoholism; 2009

RESEARCH SOCIETY ON ALCOHOLISM

Participation of Opioid System in Acquisition of Prenatal Ethanol-related Memories: effects upon neonatal and infantile responsiveness to the drug R.S. Miranda Morales, J.C. Molina, N.E. Spear and P. Abate. Instituto Ferreyra, Córdoba Capital, CP 5016, Córdoba, Argentina. Facultad de Psicología. CP 5000, Córdoba, Argentina. Center for Developmental Psychobiology – SUNY, Binghamton, NY 13902-600, USA. The main goal of this study was to analyze the involvement of the opioid system in the acquisition and expression of a prenatal ethanol-related memory. We evaluated how this prenatal experience modulates ethanol self-administration in newborn rats, and infantile ingestion of the drug. During GD’s 17-20, four groups of dams were treated with ethanol or water and immediately after they receive a naloxone or saline injection; a fifth prenatal group received naloxone 20-min before ethanol administration. On PD 1, pups were evaluated in an operant learning task to obtain milk or EtOH 3% (FR=1). Yoked controls received the reinforcer when paired pup was rewarded. During extinction, reinforcer was not available. At PD14 and 15, the remaining pups were evaluated in an intake test with infusions of ethanol at 5% or water. On PD14 before intake test, infants received a treatment with naloxone. At PD1 pups rapidly acquired an operant response to gain access to milk. Only pups prenatally treated with ethanol (after been exposed to maternal naloxone or saline), increased operant responses, to gain access to ethanol. This profile was similar during acquisition and extinction session. Infantile intake test showed a similar profile of response, as a function of prenatal groups. Pups prenatally exposed to ethanol and then injected with naloxone or saline, consumed higher levels of ethanol, in comparison with the remaining groups. Of major importance, prenatal naloxone injected 20-min before ethanol, significantly reduced neonatal ethanol’s operant response as well as infantile ethanol consumption. Naloxone treatment at PD14 produced a generalized reduction of intake scores. As previous evidences have indicated, ethanol prenatal experiences promote neonatal operant learning, supported by reinforcing attributes of the drug. Of major importance for this study, the opioid system mediates the acquisition of a prenatal ethanol memory. Results from infantile intake test indicate long-term retention of a prenatal ethanol-related memory. Ethanol consumption was considerably increased as a function of prenatal experience with the drug, and this preference was inhibited when the opioid system was silenced some time before prenatal ethanol presentation. Finally, it seems clear that the endogenous opioid system is involved in the acquisition of prenatal ethanol memories, and this experience can modulate reinforcing attributes of the drug in neonate and infant rats.