Chronic ad libitum ethanol exposure impairs corticolimbic and cerebellar structural neuroplasticity in rats

Consequences of chronic ethanol exposure on cognitive and motor functions are widely studied due to the neurodegeneration that ethanol produces in the cerebellum and other brain areas, including some corticolimbic regions. However, there is scarce information about the structural neuroplasticity effects of chronic ethanol exposure that ultimately lead to characteristic neurodegenerative consequences. For this purpose, we evaluated the effects of chronic ethanol exposure in adult male rats on exploratory behavior (locomotor activity induced by a novel environment) and structural neuroplasticity in corticolimbic and cerebellar neurons. After 90 days of ad libitum ethanol (10%) exposure, the locomotor behavior of the animals did not differ from that of the control group (exposed to water). Structural neuroplasticity was assessed using the Golgi-Cox technique in neurons from corticolimbic areas and the cerebellum. The findings revealed that ethanol exposure induced basilar dendritic atrophy without modifying the dendritic spine density in pyramidal cells in prefrontal cortex layers 3 and 5, the CA1 region of the dorsal hippocampus, and the basolateral amygdala. In contrast, ethanol exposure hypotrophied the dendritic arbor of Purkinje cells and reduced the density of dendritic spines in these cells. These data contribute to the knowledge of the neuroplasticity-related mechanisms underlying the neurodegenerative consequences of chronic ethanol exposure and its cognitive implications.