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A Rat Model of Mild Intrauterine Hypoperfusion with Microcoil Stenosis
Published on: January 7, 2018
Mild prenatal protein malnutrition increases alpha 2C-adrenoceptor expression in the rat cerebral cortex during
Walter Sierralta1, Alejandro Hernández, Luis Valladares
1Institute of Nutrition and Food Technology (INTA), University of Chile, Santiago, Chile.
Insights
Mild prenatal protein deficiency in rats increased alpha 2C-adrenoceptor expression in the cortex during early postnatal life. This overexpression may explain neural and behavioral issues observed in malnourished pups.
Area of Science:
- Neuroscience
- Developmental Biology
- Nutritional Science
Background:
- Prenatal protein malnutrition can impact offspring neurodevelopment.
- Noradrenergic system and alpha-2C-adrenoceptors play roles in neuroplasticity and cognitive functions.
Purpose of the Study:
- To investigate the effect of mild prenatal protein malnutrition on alpha 2C-adrenoceptor expression in rat cortices.
- To correlate these changes with observed neural and behavioral disturbances.
Main Methods:
- Utilized immunohistochemical methods to assess alpha 2C-adrenoceptor expression.
- Examined expression in frontal and occipital cortices of 8- and 60-day-old rats.
- Compared prenatally malnourished rats with well-nourished controls.
Main Results:
- An approximate three-fold increase in alpha 2C-adrenoceptor expression was observed in the cortices of 8-day-old malnourished rats.
- By postnatal day 60, alpha 2C-adrenoceptor expression levels returned to normal in the neocortex.
- Prenatal protein restriction altered cortical noradrenaline levels and impaired long-term potentiation and memory.
Conclusions:
- Mild prenatal protein malnutrition leads to a transient overexpression of neocortical alpha 2C-adrenoceptors in early postnatal life.
- This early-life overexpression may contribute to the neural and behavioral deficits observed in malnourished offspring.
- Understanding these mechanisms is crucial for addressing developmental consequences of maternal nutritional deficiencies.
Abstract:
Mild reduction in the protein content in the diet of pregnant rats from 25 to 8% casein, calorically compensated by carbohydrates, does not alter body and brain weights of rat pups at birth, but results in significant changes of the concentration and release of cortical noradrenaline during postnatal life, together with impaired long-term potentiation and memory formation. Since some central noradrenergic receptors are critically involved in neuroplasticity, the present study evaluated, by utilizing immunohistochemical methods, the effect of mild prenatal protein malnutrition on the alpha 2C-adrenoceptor expression in the frontal and occipital cortices of 8- and 60-day-old rats. At day 8 of postnatal age, prenatally malnourished rats exhibited a three-fold increase of alpha 2C-adrenoceptor expression in both the frontal and the occipital cortices, as compared to well-nourished controls. At 60 days of age, prenatally malnourished rats showed normal expression levels scores of alpha 2C-adrenoceptor in the neocortex. Results suggest that overexpression of neocortical alpha 2C-adrenoceptors during early postnatal life, subsequent to mild prenatal protein malnutrition, could in part be responsible for neural and behavioral disturbances showing prenatally malnourished animals during the postnatal life.
