Early exposure to stressful stimuli is crucial for developing varied behavioural patterns in adulthood such as anxiety, cognitive dysfunction and abuse disorders. The alteration of the hypothalamic–pitu-itary-adrenal (HPA) axis represents the neurobiological substrate responsible of the behavioural consequences of prenatal stress (PS). Indeed, prenatal manipulation of the HPA axis impacts on cognitive performance of the adult offspring, but also on vulnerability to alcohol consumption. Based upon these findings, we aimed at assessing the impact of a single, intense prenatal stress on exposure to alcohol preference and on the effects exerted by ethanol on behavioural reactivity, anxiety-like behaviour and spatial learning in adult male Wistar rats. Our study proved that both alcohol free- access (PS-FA)and free-access (FA) groups had an irregular trend in alcohol consumption, representing an initial binge-like drinking behaviour, then ensued by a voluntary reduction in alcohol intake to moderate values, evidencing that prenatal stress does not influence ethanol consumption in adulthood.Moderate ethanol intake exerts anxiolytic properties, as showed by the OFT and EPM, improving the response to stress in the adversative situation in the MWM. Furthermore, ethanol facilitating effect on cognitive performance was enhanced by prenatal attenuation of HPA axis. Indeed, corticosterone levels are inversely correlated with mechanisms of hippocampal neuroplasticity such as BDNF release. In conclusion, our findings further highlight the role of prenatal experiences on ethanol-induced mechanisms of neuroadaptation.
|Numero di pagine||2|
|Stato di pubblicazione||Published - 2015|
All Science Journal Classification (ASJC) codes