Yan Peng, Liu Jincen, Ma Haotian, Feng Yue, Cui Jingjing, Bai Yuying, Huang Xin, Zhu Yongsheng, Wei Shuguang, Lai Jianghua
NHC Key Laboratory of Forensic Science, School of Forensic Sciences, Xi'an Jiaotong University, Xi'an, China.
Forensic Identification Institute, The Fourth People's Hospital of Yancheng, Yancheng, China.
Front Mol Neurosci. 2023 Mar 6;16:1129553. doi: 10.3389/fnmol.2023.1129553. eCollection 2023.
Glycogen synthase kinase-3β (GSK3β) has been implicated in the maintenance of synaptic plasticity, memory process, and psychostimulant-induced behavioral effects. Hyperactive GSK3β in the Cornu Ammonis 1 (CA1) subregion of the dorsal hippocampus (DHP) was associated with adolescent methamphetamine (METH) exposure-induced behavioral and cognitive deficits in adulthood. This study aimed to evaluate the possible therapeutic effects of GSK3β inhibition in adulthood on adolescent METH exposure-induced long-term neurobiological deficits.
Adolescent male mice were treated with METH from postnatal day (PND) 45-51. In adulthood, three intervention protocols (acute lithium chloride systemic administration, chronic lithium chloride systemic administration, and chronic SB216763 administration within CA1) were used for GSK3β activity inhibition. The effect of GSK3β intervention on cognition, behavior, and GSK3β activity and synaptic ultrastructure in the DHP CA1 subregion were detected in adulthood.
In adulthood, all three interventions reduced adolescent METH exposure-induced hyperactivity (PND97), while only chronic systemic and chronic within CA1 administration ameliorated the induced impairments in spatial (PND99), social (PND101) and object (PND103) recognition memory. In addition, although three interventions reversed the aberrant GSK3β activity in the DHP CA1 subregion (PND104), only chronic systemic and chronic within CA1 administration rescued adolescent METH exposure-induced synaptic ultrastructure changes in the DHP CA1 subregion (PND104) in adulthood.
Rescuing synaptic ultrastructural abnormalities in the dHIP CA1 subregion by chronic administration of a GSK3β inhibitor may be a suitable therapeutic strategy for the treatment of behavioral and cognitive deficits in adulthood associated with adolescent METH abuse.
糖原合酶激酶-3β(GSK3β)与突触可塑性的维持、记忆过程以及精神兴奋剂诱导的行为效应有关。背侧海马体(DHP)角回1(CA1)亚区中GSK3β活性过高与青少年期接触甲基苯丙胺(METH)所致成年期行为和认知缺陷有关。本研究旨在评估成年期抑制GSK3β对青少年期接触METH所致长期神经生物学缺陷的可能治疗作用。
从出生后第45天至第51天对青春期雄性小鼠进行METH处理。成年后,采用三种干预方案(急性氯化锂全身给药、慢性氯化锂全身给药以及在CA1区域内慢性给予SB216763)抑制GSK3β活性。在成年期检测GSK3β干预对DHP CA1亚区认知、行为、GSK3β活性及突触超微结构的影响。
成年期,所有三种干预均降低了青少年期接触METH所致的多动(出生后第97天),而只有慢性全身给药和CA1区域内慢性给药改善了诱导的空间(出生后第99天)、社交(出生后第101天)和物体(出生后第103天)识别记忆损伤。此外,虽然三种干预均逆转了DHP CA1亚区异常的GSK3β活性(出生后第104天),但只有慢性全身给药和CA1区域内慢性给药挽救了成年期青少年期接触METH所致的DHP CA1亚区突触超微结构变化(出生后第104天)。
通过长期给予GSK3β抑制剂挽救dHIP CA1亚区的突触超微结构异常可能是治疗成年期与青少年期METH滥用相关行为和认知缺陷的合适治疗策略。