CONICET | Buscador de Institutos y Recursos Humanos

INVESTIGADORES

ABATE Paula

datos académicos

artículos

capítulos de libros

congresos y reuniones científicas

Título:

Participation of opioid system in acquisition of prenatal ethanol related memories: effects upon neonatal and infantile responsiveness to the drug

Autor/es:

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

Lugar:

SAN DIEGO, EEUU

Reunión:

Congreso; 2009 Scientific Meeting of the Research Society on Alcoholism. RSA, EEUU; 2009

Institución organizadora:

RESEARCH SOCIETY ON ALCOHOLISM

Resumen:

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 gestational days 17-20, four groups of dams were treated with ethanol or water and immediately after they receive a non-selective opioid antagonist (naloxone) or saline injection; a fifth prenatal group received naloxone 20-min before ethanol administration. On postnatal day (PD) 1, pups were evaluated in an operant learning procedure. Neonates were trained to obtain a given reward (milk or 3% EtOH v/v) in a FR=1 schedule. Yoked control pups received the reinforcer each time the experimental pup was rewarded. During the extinction session, reinforcer was not available. During infancy (PD14 and 15), pups representative from each prenatal treatment were evaluated in an intake test with infusions of ethanol at 5% or water. On PD14 before intake test, infants received a postnatal treatment with naloxone. One day old pups, independently from prenatal treatment, rapidly acquired an operant response to gain access to milk. Only pups prenatally treated with ethanol, and immediately after exposed to maternal naloxone or saline injection, increased operant responses, to gain access to ethanol. This profile was similar during acquisition and extinction session. Intake test during infancy showed a similar profile of response, as a function of prenatal groups. Those pups prenatally exposed to ethanol and then injected with naloxone or saline, consumed higher levels of ethanol, in comparison with the remaining groups. Prenatal naloxone treatment, injected before ethanol administration, significantly reduced ethanol consumption during infancy. Postnatal treatment with naloxone did not interact with prenatal experiences. This substance exerted a generalized decrement of intake consumption at PD14.  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 gestational days 17-20, four groups of dams were treated with ethanol or water and immediately after they receive a non-selective opioid antagonist (naloxone) or saline injection; a fifth prenatal group received naloxone 20-min before ethanol administration. On postnatal day (PD) 1, pups were evaluated in an operant learning procedure. Neonates were trained to obtain a given reward (milk or 3% EtOH v/v) in a FR=1 schedule. Yoked control pups received the reinforcer each time the experimental pup was rewarded. During the extinction session, reinforcer was not available. During infancy (PD14 and 15), pups representative from each prenatal treatment were evaluated in an intake test with infusions of ethanol at 5% or water. On PD14 before intake test, infants received a postnatal treatment with naloxone. One day old pups, independently from prenatal treatment, rapidly acquired an operant response to gain access to milk. Only pups prenatally treated with ethanol, and immediately after exposed to maternal naloxone or saline injection, increased operant responses, to gain access to ethanol. This profile was similar during acquisition and extinction session. Intake test during infancy showed a similar profile of response, as a function of prenatal groups. Those pups prenatally exposed to ethanol and then injected with naloxone or saline, consumed higher levels of ethanol, in comparison with the remaining groups. Prenatal naloxone treatment, injected before ethanol administration, significantly reduced ethanol consumption during infancy. Postnatal treatment with naloxone did not interact with prenatal experiences. This substance exerted a generalized decrement of intake consumption at PD14. These results extend previous results indicating that ethanol prenatal experiences promote neonatal operant learning, supported by reinforcing attributes of the drug. Of mayor importance for this study, we also observed that the endogenous opioid system is involved in the acquisition of this prenatal ethanol-related memory, particularly when this neurobiological system is already blocked 20-min before ethanol presentation. 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. Similar that was observed at PD1, this preference for ethanol consumption 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.

enviar mensaje