Learning experiences comprising central ethanol exposure in rat neonates: Impact upon respiratory plasticity and the activity of brain catalase

Moderate ethanol exposure during early ontogeny of the rat alters respiratory plasticity, ultrasonic distress vocalizations, increases brain catalase activity, and acetaldehyde-mediated ethanol intake

“…In addition, those pups that received mixed milk with ethanol twice (i.e., E-E) showed significantly fewer apneic episodes compared to the groups that received milk as the sole liquid (i.e., M-M and E-M). The latter findings go in line with previous studies indicating that the mere -central or peripheral- experience with ethanol during PDs 3–9 attenuates apneic episodes induced by stress-related factors, suggesting early ethanol’s anxiolytic effects if the experience with the drug occurs postnatally ( D’aloisio et al, 2020 ; Trujillo et al, 2020 ; Anunziata et al, 2021 ). Given the scarce pup’s behavioral repertoire and the lack of tests adjusted to age, both apneic episodes and latency to emit them may serve as proxies for animals’ anxiety levels.…”

“…In addition, pups showed lower breathing frequencies until an apneic episode occurred (coefficient breaths/apneas, Figure 2C ). Regardless of the treatment’s nature, a transient decrease in breathing frequencies ( Figure 2A ) was observed throughout evaluations, indicative of a habituation process ( Macchione et al, 2016 , 2018 , 2021 ; Acevedo et al, 2017a , b ; D’aloisio et al, 2020 ; Trujillo et al, 2020 ). The short and long-term effects of ethanol on neonatal respiratory plasticity more recently have received attention given the association between fetal alcohol exposure and the sudden infant death syndrome ( Iyasu et al, 2002 ; Burd et al, 2004 ; Bailey and Sokol, 2011 ; O’Leary et al, 2013 ).…”

“…About 60% of this enzymatic system is mainly responsible for metabolizing ethanol into acetaldehyde in the brain ( Aragon et al, 1991b ; Zimatkin et al, 2006 ) and its peak levels of activity occurs from late gestational period to the first week after birth ( Del Maestro and McDonald, 1987 ). It seems that repeated experiences with high ethanol doses are necessary to induce such brain catalase activity ( Hamby-Mason et al, 1997 ; Trujillo et al, 2020 ). Not only high but also moderate ethanol exposures, as we observed here, activate the enzymatic system.…”

“…The resultant activity was expressed as units of catalase activity (mmol H 2 O 2 /min/mg of protein). Similar protocols to estimate catalase activity has been performed in previous studies (Correa et al, 2001;Klongpityapong et al, 2013;Mattalloni et al, 2013;Carvajal-Serna et al, 2020;Trujillo et al, 2020).…”

“…The intragastric experience with low doses of ethanol (0.25, 0.5, or 1.25 g/kg) during PD 14 reduces an odor avoidance response at PD 15 ( Pautassi et al, 2006 ) and increases the time spent in the illuminated area in a light/dark box test with a 0.5 g/kg ethanol dose at PD 16 ( Miranda-Morales et al, 2014 ). Recent studies also suggested that early anxiolytic effects of ethanol, as apneic episodes during PDs 3–7 are reduced after repeated intracisternal administrations of a high ethanol dose (300 mg%, Trujillo et al, 2020 ) and after intragastric administrations of low or moderate ethanol doses (0.75, 1.37, and 2.0 g/kg) during PDs 3–9 ( D’aloisio et al, 2020 ; Anunziata et al, 2021 ). Binge-like ethanol exposure (3.0 g/kg) during PDs 4–10 decreases ultrasonic vocalizations (USVs) – considered as a proxy of anxiety- on PD 14 ( Barron and Gilbertson, 2005 ) and a low dose of ethanol (0.5 g/kg) exerts a protected effect on maternal separation stress-induced vocalizations on PD 14 ( Pautassi et al, 2007 ).…”