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

Authors

  • Claudia Rebeca Mendoza (1) Laboratorio de Neuropsiquiatría, Instituto de Fisiología, Benemérita Universidad Autónoma de Puebla (BUAP), Puebla, Mexico. (2) Escuela Nacional de Ciencias Biológicas (ENCB), Instituto Politécnico Nacional (IPN), Mexico City, Mexico.
  • Leonardo Aguilar-Hernández Laboratorio de Neuropsiquiatría, Instituto de Fisiología, Benemérita Universidad Autónoma de Puebla (BUAP), Puebla, Mexico.
  • David J. Apam-Castillejos Laboratorio de Neuropsiquiatría, Instituto de Fisiología, Benemérita Universidad Autónoma de Puebla (BUAP), Puebla, Mexico.
  • Andrea Judith Vázquez-Hernández Laboratorio de Neuropsiquiatría, Instituto de Fisiología, Benemérita Universidad Autónoma de Puebla (BUAP), Puebla, Mexico.
  • Alfonso Díaz Laboratorio de Neuropsiquiatría, Instituto de Fisiología, Benemérita Universidad Autónoma de Puebla (BUAP), Puebla, Mexico.
  • Hiram Tendilla-Beltrán Centro de Investigación en Reproducción Animal, Cinvestav-Universidad Autónoma de Tlaxcala, Tlaxcala, Mexico.
  • Gonzalo Flores Laboratorio de Neuropsiquiatría, Instituto de Fisiología, Benemérita Universidad Autónoma de Puebla (BUAP), Puebla, Mexico.
  • Fidel de la Cruz-López Escuela Nacional de Ciencias Biológicas (ENCB), Instituto Politécnico Nacional (IPN), Mexico City, Mexico.

DOI:

https://doi.org/10.31117/neuroscirn.v9i1.472

Keywords:

Dendritic spines, Pyramidal neurons, Purkinje cells, Corticolimbic, Alcohol use disorder

Abstract

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.

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References

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Published

2026-01-05

How to Cite

Mendoza, C. R., Aguilar-Hernández, L., Apam-Castillejos, D. J., Vázquez-Hernández, A. J., Díaz, A., Tendilla-Beltrán, H., Flores, G., & de la Cruz-López, F. (2026). Chronic ad libitum ethanol exposure impairs corticolimbic and cerebellar structural neuroplasticity in rats. Neuroscience Research Notes, 9(1), 472.1–472.14. https://doi.org/10.31117/neuroscirn.v9i1.472