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Long term reduction in eight arm maze performance after early exposure to phenobarbital
1Department of Anatomy and Embryology, Hebrew University-Hadassah Medical School, P.O. Box 1172, Jerusalem, Israel.
Insights
Early exposure to phenobarbital (PhB) significantly impairs hippocampal function in mice. This neurodevelopmental deficit affects spatial learning and memory, as evidenced by maze performance.
Area of Science:
- Neuroscience
- Developmental Toxicology
- Behavioral Pharmacology
Background:
- Previous research suggests early phenobarbital (PhB) exposure may lead to hippocampal neural deficits.
- The hippocampus is crucial for learning and memory processes.
Purpose of the Study:
- To investigate the impact of early phenobarbital exposure on hippocampal-dependent spatial learning and memory in mice.
- To quantify performance deficits in an eight-arm maze following prenatal and neonatal PhB exposure.
Main Methods:
- Mice were exposed to phenobarbital (PhB) either prenatally (via maternal diet) or neonatally (via injection).
- Spatial learning and memory were assessed using an eight-arm maze task at 50 days of age.
- Performance was evaluated based on correct entries, trials to criterion, and time to reach criterion.
Main Results:
- Mice exposed to PhB early in development exhibited significant deficits in eight-arm maze performance.
- Prenatally exposed mice showed a 12% reduction in correct entries and required 27% more trials to criterion.
- Neonatally exposed mice demonstrated a 10% reduction in correct entries and needed 13% more trials to criterion.
Conclusions:
- Early phenobarbital exposure, both prenatal and neonatal, induces lasting deficits in hippocampal-dependent spatial learning and memory.
- These findings highlight the neurodevelopmental toxicity of phenobarbital during critical early life periods.
Abstract:
Performance in the hippocampal eight arm maze was studied in mice after early exposure to phenobarbital (PhB). since previous studies suggested that these animals suffered neural deficits in the hippocampus. For prenatal exposure pregnant mothers were fed 3 g PhB/kg milled food on gestation days 9-18. Neonates were injected daily with 50 mg PhB/kg. on postnatal days 2-21. After a week of water deprivation, the animals were tested at age 50 days for 5 days preceded by 1 day of habituation. Deficits in eight arm maze performance were demonstrated in early treated mice on every testing day. For example, on day 5 of testing the number of correct entries during the first eight attempts in the prenatally treated group were 12% below control level (P<0.01), the respective reduction in the neonatal group was 10% (P< 0.001). The number of trials needed to enter all arms on day 5 was 27% above control level among prenatally treated mice (P< 0.001), and 13% in neonatally treated mice (P< 0.05). It took prenatal PhB animals twice the time to reach criterion than their controls (P< 0.001) and four times as long for neonatally treated mice (P< 0.001).
