Journal of psychopharmacology (Oxford, England) · 2025
Effects of electroconvulsive shock on astroglial reactivity in a rat model of antipsychotic-induced neurotoxicity.
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Hirose Yuki, Oda Yasunori, Yano Fumiaki, Yamasaki Fumiaki, Nakata Yusuke, Shirayama Yukihiko, Niitsu Tomihisa
Аннотация
OBJECTIVES: Electroconvulsive shock (ES) can ameliorate psychotic symptoms and certain adverse effects of antipsychotics by inducing seizure activity via electrical brain stimulation. Although the relationship between ES and glial cells has been the focus of attention, the precise mechanisms underlying its effects remain unclear. This study aimed to investigate the effects of ES on astroglia in the drug-induced neurotoxicity rat model.
METHODS: Haloperidol (HAL; 0.75 mg/kg/day for 28 days) or vehicle was administered to rats via an osmotic mini-pump, then received repeated seizure-inducing electrical stimulus (80 mA, 100 Hz, for 1 seconds with a pulse width of 0.5 mseconds) or sham operation twice daily for five consecutive days. The levels of glial fibrillary acidic protein (GFAP), glutamate transporter-1, and glutamine synthetase were determined in the brain regions.
RESULTS: ES treatment led to GFAP expression, which is indicative of astrocyte activation. In the CA1 region, astrocytic changes associated with neurotoxicity were observed in the HAL-treated group. Furthermore, astroglial reactivity in this region was ameliorated following ES.
CONCLUSIONS: The present study suggests that ES could activate the astrocytic system. Furthermore, our results also showed that ES may mitigate neurotoxic damage induced by antipsychotics. In view of the need for therapeutic strategies for treatment-resistant psychiatric disorders, further investigations of our findings are warranted.
METHODS: Haloperidol (HAL; 0.75 mg/kg/day for 28 days) or vehicle was administered to rats via an osmotic mini-pump, then received repeated seizure-inducing electrical stimulus (80 mA, 100 Hz, for 1 seconds with a pulse width of 0.5 mseconds) or sham operation twice daily for five consecutive days. The levels of glial fibrillary acidic protein (GFAP), glutamate transporter-1, and glutamine synthetase were determined in the brain regions.
RESULTS: ES treatment led to GFAP expression, which is indicative of astrocyte activation. In the CA1 region, astrocytic changes associated with neurotoxicity were observed in the HAL-treated group. Furthermore, astroglial reactivity in this region was ameliorated following ES.
CONCLUSIONS: The present study suggests that ES could activate the astrocytic system. Furthermore, our results also showed that ES may mitigate neurotoxic damage induced by antipsychotics. In view of the need for therapeutic strategies for treatment-resistant psychiatric disorders, further investigations of our findings are warranted.