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Immunohistochemical Visualization of Hippocampal Neuron Activity After Spatial Learning in a Mouse Model of Neurodevelopmental Disorders
Published on: May 12, 2015
Hippocampal apoptosis involved in learning deficits in the offspring exposed to maternal high sucrose diets
Hanzhe Kuang1, Miao Sun1, Juanxiu Lv1
1Institute for Fetology, The First Affiliated Hospital of Soochow University, Suzhou 215006, China.
Insights
Maternal high sucrose diets during pregnancy impaired offspring learning and memory. This was linked to increased hippocampal cell death and altered key protein levels, suggesting a role in cognitive disorders.
Area of Science:
- Neuroscience
- Developmental Biology
- Metabolic Disorders
Background:
- The hippocampus is vital for learning and memory; its neuronal apoptosis causes deficits.
- Maternal metabolic issues, like high sugar intake, can impact offspring brain development and cognitive functions.
Purpose of the Study:
- To investigate the effects of maternal high sucrose (HS) diets on the behavior and hippocampal neurons of young offspring.
- To understand the molecular mechanisms underlying cognitive deficits induced by prenatal HS exposure.
Main Methods:
- Offspring exposed to maternal HS diets were assessed for brain-to-body weight ratio and spatial learning using the Morris water maze.
- Hippocampal tissues were analyzed for neuronal apoptosis (TUNEL assay) and protein expression (IGF-I, PI3K, Akt, caspase-3, NMDAR, Bcl-2).
Main Results:
- Prenatal HS exposure decreased offspring brain-to-body weight ratio and impaired spatial learning (increased escape latency and path length).
- Increased TUNEL-positive cells in hippocampal subfields (CA1, CA2, CA3) indicated significant apoptosis.
- Decreased expression of anti-apoptotic factors (IGF-I, PI3K, p-Akt) and increased pro-apoptotic factors (caspase-3, NMDAR) were observed.
Conclusions:
- Maternal high sucrose diets induce spatial acquisition deficits in offspring, associated with hippocampal apoptosis.
- Altered anti-apoptotic signaling in the hippocampus may be a critical factor in cognitive disorders in children exposed to high sugar during development.
Abstract:
The hippocampus plays a crucial role in learning and memory, and neuronal apoptosis in the hippocampus contributes to learning deficits. Metabolism problems in pregnancy related to excessive fuel consumption (e.g., high fat, high sugar) may influence cognitive and behavioral functions in the offspring by affecting developing brain cells. This study determined the influence of maternal high sucrose (HS) diets on behavior and hippocampal neurons in the young offspring. The ratio of brain weight to body weight in the offspring exposed to prenatal HS diets was significantly decreased; the Morris water maze showed that the offspring exposed to prenatal HS diets exhibited increased escape latencies and path length during navigation testing, while there were no changes in time spent in the target quadrant and number of target approaches. In the offspring exposed to prenatal HS, TUNEL-positive cells were significantly increased in CA1, CA2 and CA3 of the hippocampus; protein expression of insulin-like growth factor-I, PI3K and phosphorylated Akt was significantly decreased, while caspase-3 and N-methyl-d-aspartate receptors were significantly increased in the hippocampus, and there was no change in expression of Bcl-2 and Akt. The results demonstrated that prenatal HS diets could induce the spatial acquisition deficits in the young offspring associated with hippocampal apoptosis, and altered signaling factors for antiapoptosis in the hippocampus might play a critical role in cognition disorders in young children.
