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

Fetal ethanol exposure represents a risk factor for sudden infant death syndrome, and the respiratory effects of fetal ethanol exposure promote hypoxic ischemic consequences. This study analyzes central ethanol's effects upon breathing plasticity during an ontogenetic stage equivalent to the human third gestational trimester. Ethanol's unconditioned breathing effects and their intervention in learning processes were examined. Since central ethanol is primarily metabolized via the catalase system, we also examined the effects of early history with the drug upon this system. During postnatal days 3, 5, and 7 (PDs 3-7), pups were intracisternally administered with vehicle or ethanol (300 mg%). They were tested in a plethysmograph scented or not scented with ethanol odor. The state of intoxication attenuated the onset of apneas, a phenomenon that is suggestive of ethanol's anxiolytic effects given the state of arousal caused by the novel environment and the stress of ethanol administration. At PD9, pups were evaluated when sober under sequential air conditions (initial-normoxia, hypoxia, and recovery-normoxia), with or without the presence of ethanol odor. Initial apneic episodes increased when ethanol intoxication was previously associated with the odor. Pups then ingested ethanol, and brain catalase activity was determined. Pre-exposure to ethanol intoxication paired with the odor of the drug resulted in heightened enzymatic activity. Central ethanol exposure appears to exert antianxiety effects that attenuate apneic disruptions. However, during withdrawal, the cues associated with such effects elicit an opposite reaction. The activity of the catalase system was also dependent upon learning processes that involved the association of environmental stimuli and ethanol intoxication.