Timothy B Johnson1, Charles R Goodlett. 1. Department of Psychology, Indiana University-Purdue University Indianapolis, Indianapolis, Indiana 46202-3275, USA.
Abstract
BACKGROUND: In rats, heavy bingelike alcohol exposure during the neonatal brain growth spurt [postnatal days (PD) 4-9] can impair development of spatial learning. This study tested whether binge exposure limited to the latter half of this period (PD 7-9) produced selective spatial learning deficits that endured into adulthood. METHODS: On PD 7 to 9, Long-Evans rats were given intubations of alcohol (5.25 g/kg/day), sham intubations, or no intubations. Rats were tested as adults (>or=PD 70) in the Morris water maze under one of three different conditions: place (submerged escape platform in the same location each trial), random (submerged platform in a different, random location each trial), or redundant (visible platform that protruded above the water, in the same location for each trial). A 60-sec probe trial (with no platform present) followed the last acquisition trial. RESULTS: The mean peak blood alcohol concentration was 401 mg/dl on PD 7. Neonatal alcohol treatment significantly impaired acquisition and reduced place biases on the probe trial in place-trained males, but not females. Neonatal alcohol treatment had no significant effects on acquisition performance of the random or redundant groups. Redundant training yielded rapid acquisition for all groups. The visible cue overshadowed place cues for all treatment groups, but small place biases were evident in controls. After random training, no group showed place biases. CONCLUSIONS: Heavy alcohol exposure in rats limited to the last half of the neonatal brain growth spurt caused enduring deficits in spatial learning, but only in males. The deficits were specific to place learning in the Morris water maze and emerged only when learning and performance depended on the use of distal place cues.
BACKGROUND: In rats, heavy bingelike alcohol exposure during the neonatal brain growth spurt [postnatal days (PD) 4-9] can impair development of spatial learning. This study tested whether binge exposure limited to the latter half of this period (PD 7-9) produced selective spatial learning deficits that endured into adulthood. METHODS: On PD 7 to 9, Long-Evans rats were given intubations of alcohol (5.25 g/kg/day), sham intubations, or no intubations. Rats were tested as adults (>or=PD 70) in the Morris water maze under one of three different conditions: place (submerged escape platform in the same location each trial), random (submerged platform in a different, random location each trial), or redundant (visible platform that protruded above the water, in the same location for each trial). A 60-sec probe trial (with no platform present) followed the last acquisition trial. RESULTS: The mean peak blood alcohol concentration was 401 mg/dl on PD 7. Neonatal alcohol treatment significantly impaired acquisition and reduced place biases on the probe trial in place-trained males, but not females. Neonatal alcohol treatment had no significant effects on acquisition performance of the random or redundant groups. Redundant training yielded rapid acquisition for all groups. The visible cue overshadowed place cues for all treatment groups, but small place biases were evident in controls. After random training, no group showed place biases. CONCLUSIONS: Heavy alcohol exposure in rats limited to the last half of the neonatal brain growth spurt caused enduring deficits in spatial learning, but only in males. The deficits were specific to place learning in the Morris water maze and emerged only when learning and performance depended on the use of distal place cues.
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