Prenatal alcohol exposure induces anxiety and depressive-like behaviors with deficits in growth and food intake in mice

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Background/Objectives: Prenatal alcohol exposure (PAE) has been recognized as a significant public health concern due to its consequential and long-lasting effects on the central nervous system (CNS) and the subsequent behavioral impairments in affected individuals. The current study aims to evaluate postnatal neurobehavioral disturbances, specifically mood state and potential morpho-functional changes, as well as brain oxidative stress in mice prenatally intoxicated with ethanol at the adult stage. Methods: female mice with positive vaginal plugs were divided into three groups: Group 1 (ethanol intoxicated): received ethanol at a dose of 1 g/kg (i.p.) on gestational days 10 and 13 (two injections in total), along with pyrazole (100 mg/kg by i. p.) to inhibit ethanol metabolism and simulate chronic fetal exposure. The second group received pyrazole alone at the same dose (100 mg/kg i. p.). Group 3 (controls): received physiological saline solution (NaCl 0.9%) at the same volume as both ethanol and pyrazole. Offspring pups from the intoxicated dams were subjected, at the adult stage (from postnatal days P95 to P103), to a series of morphometric, biometric, neurobehavioral, and biochemical analyses. Results: Our data show an obvious decrease in body weight and size, decreased food intake, and skeleton deformations. Additionally, PAE mice exacerbated anxiety-like and depressive-like behaviors as well as elevated brain oxidative stress. Conclusion: The current data demonstrate the powerful neurotoxic effect of prenatal ethanol exposure on neuropsychological development as well as the associated morpho-functional changes.

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