Exposição gestacional aguda ao etanol em ratos wistar: alterações comportamentais e hidroeletrolíticas

Abstract

The acute gestational exposure to ethanol can cause disorders in the development of several systems of neurotransmitters, promoting functional changes that may persist for all life of individual. In the present work, we evaluated the acute prenatal influence of ethanol on hydroelectrolytic regulation and various behavioral and ontogenetic responses related to brain serotonergic system. The hydroelectrolytic regulation is critical to the development of numerous biochemical processes related to the maintenance of life, and one of the main adaptive mechanisms involved in the conquest of the terrestrial environment. The brain serotonergic system has a critical role in the maintenance of fluid and electrolyte homeostasis, particularly in the satiety sodium behavior. Assuredly, the pattern of serotonergic activity may be critically affected by xenobiotics during embryonic neurogenesis. The ethanol administration during pregnancy reduces serotonin synthesis and tryptophan hydroxylase expression in Dorsal Raphe Nucleus in rats. Although previously studies shown that ethanol gestational exposure generate damage on serotonergic circuits, had not hitherto data reporting the influence this exposure on the mechanisms of hydroelctrolytic homeostasis, especially acute treatments that have more tangible translational aspect. In this context, the present study aimed to assert the spectrum of possible alterations triggered by acute prenatal exposure to ethanol on the sodium appetite and other parameters involved in electrolytic control, as well as other behavioral responses. For this, in 14th day of pregnancy, female rats were treated with ethanol solution (20% in saline solution, 3 g/kg, i.p.). At ninety day of life, groups of at least 10 individuals from different mothers were randomly assigned to conduct the experimental manipulations. At this age, the cumulative intake of sodium and water was measured after four days of low-sodium diet and after administration of 10 mg/kg of furosemide (s.c.) associated with captopril (5 mg/kg s.c.). In this same experimental paradigm, we also evaluated the evolution of body weight, systolic blood pressure, glomerular filtration rate, urinary and plasma sodium concentration and hematocrit of the groups. The ethanol group showed higher cumulative sodium intake, but no significant differences in the other parameters described. We also investigated the neuronal activation (by immunoreactivity to Fos) of the main brain structures involved in the control of salt intake. Animals of ethanol group showed higher number of Fos-ir cells in the OVLT and SFO during the consumption phase, and no difference in number of immunoreactivity cells in MnPO, and reduced ir-Fos in SON, PVN (PaML, PaMM, PaPo) and DRN, indicate lower reactivity in these areas after ingestion of salt. We also demonstrated that the animals of ethanol group showed anxiety-like behavior and deficit in consolidation and evocation of memory. However, ethanol treatment does not promote sensory deficits, impairments in motor coordination and weight development, and no generates no anhedonia under baseline conditions. Our results suggest that acute prenatal ethanol exposure induces disturbances in the generation of sodium satiety behavior, anxiety-like behaviour and debilitates in the memory mechanisms.