Pre and postnatal alcohol exposure delays, in female but not in male rats, the extinction of an auditory fear conditioned memory and increases alcohol consumption

PLAZA, WLADIMIR; SANTIBAÑEZ, NICOLÁS; DE LA FUENTE?ORTEGA, ERWIN; GASCHINO, FELICE; ESTAY?OLMOS, CAMILA; PAUTASSI, RICARDO M.; GUTIERREZ, CAMILO; SOTOMAYOR?ZÁRATE, RAMÓN; HAEGER, PAOLA A.

DEVELOPMENTAL PSYCHOBIOLOGY

JOHN WILEY & SONS INC

Lugar: New York; Año: 2020 vol. 62 p. 519 - 531

0012-1630

Repeated exposure to alcohol increases retrieval of fear-conditioned memory, which facilitates the emergence of post-traumatic stress disorder (PTSD). Individuals with PTSD, in turn, are more likely to develop alcohol and substance abuse related disorders, and substance abusers are at high risk of experiencing potential traumatic experiences. We assessed if prenatal and early postnatal alcohol exposure (PAE) increases the susceptibility to retain aversive memories and if this is associated with subsequent heightened alcohol consumption. Pregnant Sprague-Dawley rats were exposed for 22 hours/day, from gestational day 0, throughout pregnancy, and until postnatal day 7 to a single bottle of 10% alcohol (mixed in tap water and 64mg/L of sucralose, PAE Group), or to a single bottle of tap water and sucralose (Control Group). Auditory fear conditioning (AFC) was performed in the offspring, at postnatal day 40 (PND 40). Freezing was measured during acquisition, retention and extinction (days 1, 2 and 9, respectively). Alcohol intake (preference vs. water and grams of alcohol consumed) was measured every two days for 3 weeks after the extinction test. Female, but not male, PAE rats exhibited deficits in the extinction of the aversive memory, and this result was associated with lower levels of 3-4 Dihidroxyphenylacetic acid (DOPAC) in the nucleus accumbens and heightened alcohol intake. These results suggest that female PAE animals are more vulnerable to exhibit long-term retention of aversive memories and to ingest significantly more alcohol. These results have implications for the understanding of the pathogenesis of PTSD and comorbid alcohol intake.