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Prenatal exposure to betamethasone decreases anxiety in developing rats: hippocampal neuropeptide y as a target
1Department of Neurology, Albert Einstein College of Medicine, Bronx, NY 10461, USA. velisek@aecom.yu.edu
Insights
Prenatal betamethasone exposure in rats increased neuropeptide Y (NPY) in the hippocampus, reducing anxiety-like behaviors in offspring. This suggests a potential mechanism for corticosteroid side effects in development.
Area of Science:
- Neuroscience
- Developmental Biology
- Pharmacology
Background:
- Antenatal betamethasone is a critical obstetric treatment, but its long-term effects on children are not fully understood.
- Previous studies suggest potential behavioral impairments in children exposed to repeated prenatal betamethasone courses.
Purpose of the Study:
- To investigate the effects of repeated prenatal betamethasone exposure on anxiety-related behaviors and neuropeptide Y (NPY) expression in rat offspring.
- To explore the role of the hippocampus and amygdala in mediating these effects.
Main Methods:
- Pregnant rats received two betamethasone injections on day 15 of gestation.
- Immunohistochemistry was used to measure NPY expression in the hippocampus and basolateral amygdala of offspring on postnatal day 20.
- Behavioral tests (open field, horizontal bar, elevated plus maze) assessed anxiety, motor performance, and activity levels.
Main Results:
- Prenatal betamethasone exposure significantly increased NPY expression in the hippocampus, but not the amygdala, of offspring.
- Offspring exhibited decreased anxiety-like behaviors without motor impairments or altered total activity.
- Betamethasone-exposed rats showed decreased body weight, indicating long-lasting effects.
Conclusions:
- Prenatal betamethasone treatment increases hippocampal NPY, leading to reduced anxiety-related behaviors in rats.
- This suggests a specific pathway linking antenatal corticosteroids to altered anxiety in offspring.
- Animal models can help differentiate beneficial effects from side effects of antenatal corticosteroid therapy.
Abstract:
Repeated antenatal administration of betamethasone is frequently used as a life-saving treatment in obstetrics. However, limited information is available about the outcome of this therapy in children. The initial prospective studies indicate that there are behavioral impairments in children exposed to repeated courses of prenatal betamethasone during the third trimester of pregnancy. In this study, pregnant rats received two betamethasone injections on day 15 of gestation. Using immunohistochemistry, the expression of a powerful anxiolytic molecule neuropeptide Y (NPY) was determined on postnatal day (PN) 20 in the hippocampus and basolateral amygdala (structures related to anxiety and fear) of the offspring. Prenatal betamethasone exposure induced significant increases in NPY expression in the hippocampus but not in the amygdala. Indeed, behavioral tests in the offspring, between PN20 and PN22 in the open field, on the horizontal bar, and in the elevated plus maze, indicated decreases in anxiety, without impairments in motor performance or total activity. Decreased body weight in betamethasone-exposed rats confirmed long-lasting effects of prenatal exposure. Thus, prenatal betamethasone treatment consistently increases hippocampal NPY, with decreases in anxiety-related behaviors and hippocampal role in anxiety in rats. Animal models may assist in differentiation between pathways of the desired main effect of the antenatal corticosteroid treatment and pathways of unwanted side effects. This differentiation can lead to specific therapeutic interventions directed against the side effects without eliminating the beneficial main effect of the corticosteroid treatment.
