p-Nrf2/HO-1 Pathway Involved in Methamphetamine-induced Executive Dysfunction through Endoplasmic Reticulum Stress and Apoptosis in the Dorsal Striatum

Wei, Tao; Li, Junda; Wang, Yujing; Zhao, Wei; Fan, Ding; Wang, Yan; Xia, Ling-Ling; Jiang, Zedong; Song, Xun; Zhu, Yu; Shao, Wenyi; Wang, Ze; Bi, Kai; Zhang, Xiao-Chu; Jiao, Dongliang

doi:10.1007/s12640-023-00650-7

Cited by 4 publications

(1 citation statement)

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“…Henan SCXK 2020–0005) and housed ( n = 11–13 mice/cage) in a 12 h light/dark cycle, at 20–25°C, 45%–55% humidity and free access to food and water. ICR mice were widely used in biomedical research, and we used ICR mice in our previous studies, 17 so we used ICR mice in this study for the continuity of the study. The mice were allowed to adapt to the human touch for 1 week before treatment.…”

Section: Methodsmentioning

confidence: 99%

Involvement of nucleus accumbens SERCA2b in methamphetamine‐induced conditioned place preference

Wang,

Duan,

et al. 2024

Addiction Biology

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Methamphetamine (METH) is a highly addictive psycho‐stimulant that induces addictive behaviour by stimulating increased dopamine release in the nucleus accumbens (NAc). The sarco/endoplasmic reticulum calcium ion transport ATPases (SERCA or ATP2A) is a calcium ion (Ca2+) pump in the endoplasmic reticulum (ER) membrane. SERCA2b is a SERCA subtype mainly distributed in the central nervous system. This study used conditioned place preference (CPP), a translational drug reward model, to observe the effects of SERCA and SERCA2b on METH‐CPP in mice. Result suggested that the activity of SERCA was significantly decreased in NAc after METH‐CPP. Intraperitoneal SERCA agonist CDN1163 injection or bilateral CDN1163 microinjection in the NAc inhibited METH‐CPP formation. SERCA2b overexpression by the Adeno‐associated virus can reduce the DA release of NAc and inhibit METH‐CPP formation. Although microinjection of SERCA inhibitor thapsigargin in the bilateral NAc did not significantly aggravate METH‐CPP, interference with SERCA2b expression in NAc by adeno‐associated virus increased DA release and promoted METH‐CPP formation. METH reduced the SERCA ability to transport Ca2+ into the ER in SHSY5Y cells in vitro, which was reversed by CDN1163. This study revealed that METH dysregulates intracellular calcium balance by downregulating SERCA2b function, increasing DA release in NAc and inducing METH‐CPP formation. Drugs that target SERCA2b may have the potential to treat METH addiction.

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Section: Methodsmentioning

confidence: 99%