Electroconvulsive seizures for reducing voluntary ethanol consumption in a mixed-sex cohort of adult rats
4 affiliations
- 1IUNICS, University of the Balearic Islands
- 2Health Research Institute of the Balearic Islands (IdISBa)
- 3Department of Medicine, University of the Balearic Islands
- 4Red de Investigación en Atención Primaria en Adicciones (RIAPAd), ISCIII
Abstract
The use of neuromodulation techniques for the treatment of alcohol use disorder is receiving increasing attention, especially non-invasive approaches, such as repetitive transcranial magnetic stimulation or transcranial direct current stimulation, while the hypothetical use of electroconvulsive therapy remains unexplored. Given our experience with electroconvulsive seizures (ECS) for therapeutic purposes in psychopathology rodent models, we evaluated the role of ECS on reducing the increased voluntary ethanol consumption caused by adolescent ethanol exposure in our validated preclinical model. To do so, a mixed-sex cohort of rats was treated in adolescence with a binge paradigm of ethanol (2 g/kg, i.p.; 3 rounds of 2 days at 48-h intervals) or saline. Following a persistent resting period with no drug exposure until adulthood, rats were allowed to: voluntarily drink ethanol (20%) by a two-bottle choice test, for 3 days; a week later treated with ECS (95 mA for 0.6 s, 100 Hz, pulse width 0.6 ms; ear-clip electrodes) or SHAM for 5 days; and finally, a week later re-exposed to voluntarily ethanol consumption. Brains were collected 24-h after the last ethanol exposure to evaluate hippocampal toxicity markers (e.g., NeuroD, NF-L, BDNF and NF-L/BDNF ratio). The main results showed that adolescent ethanol exposure increased voluntary ethanol consumption in a mixed-sex cohort of adult rats, and that ECS could reduce the consumption. Moreover, we suggested a possible role for BDNF in the molecular events induced by ECS, especially reducing the neurotoxic ratio NF-L/BDNF. In conclusion, we provide preclinical evidence characterizing the potential use of ECS for alcohol use disorder.
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BibTeX
@article{garciacabrerizo2026electroconvulsive,
title = {{Electroconvulsive seizures for reducing voluntary ethanol consumption in a mixed-sex cohort of adult rats}},
author = {Rubén García-Cabrerizo and Pedro Bergas-Cladera and Carles Colom-Rocha and M. Julia García-Fuster},
journal = {Frontiers in Psychiatry},
year = {2026},
month = nov,
doi = {10.3389/fpsyt.2026.1954778},
url = {https://www.frontiersin.org/articles/10.3389/fpsyt.2026.1954778/full},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Electroconvulsive seizures for reducing voluntary ethanol consumption in a mixed-sex cohort of adult rats
AU - Rubén García-Cabrerizo
AU - Pedro Bergas-Cladera
AU - Carles Colom-Rocha
AU - M. Julia García-Fuster
PY - 2026
DA - 2026/11/09
JO - Frontiers in Psychiatry
DO - 10.3389/fpsyt.2026.1954778
UR - https://www.frontiersin.org/articles/10.3389/fpsyt.2026.1954778/full
AB - The use of neuromodulation techniques for the treatment of alcohol use disorder is receiving increasing attention, especially non-invasive approaches, such as repetitive transcranial magnetic stimulation or transcranial direct current stimulation, while the hypothetical use of electroconvulsive therapy remains unexplored. Given our experience with electroconvulsive seizures (ECS) for therapeutic purposes in psychopathology rodent models, we evaluated the role of ECS on reducing the increased voluntary ethanol consumption caused by adolescent ethanol exposure in our validated preclinical model. To do so, a mixed-sex cohort of rats was treated in adolescence with a binge paradigm of ethanol (2 g/kg, i.p.; 3 rounds of 2 days at 48-h intervals) or saline. Following a persistent resting period with no drug exposure until adulthood, rats were allowed to: voluntarily drink ethanol (20%) by a two-bottle choice test, for 3 days; a week later treated with ECS (95 mA for 0.6 s, 100 Hz, pulse width 0.6 ms; ear-clip electrodes) or SHAM for 5 days; and finally, a week later re-exposed to voluntarily ethanol consumption. Brains were collected 24-h after the last ethanol exposure to evaluate hippocampal toxicity markers (e.g., NeuroD, NF-L, BDNF and NF-L/BDNF ratio). The main results showed that adolescent ethanol exposure increased voluntary ethanol consumption in a mixed-sex cohort of adult rats, and that ECS could reduce the consumption. Moreover, we suggested a possible role for BDNF in the molecular events induced by ECS, especially reducing the neurotoxic ratio NF-L/BDNF. In conclusion, we provide preclinical evidence characterizing the potential use of ECS for alcohol use disorder.
SN - 1664-0640
ER -