Ginkgo biloba and vitamin E ameliorate haloperidol-induced vacuous chewingmovement and brain-derived neurotrophic factor expression in a rat tardive dyskinesia model

• Published in: Pharmacology, biochemistry and behavior biochemistry and behavior, 2016-09, Vol.148, p.53-58
• Main Authors: Shi, Jing, Tan, Yun Long, Wang, Zhi Ren, An, Hui Mei, Li, Jia, Wang, Yue Chan, Lv, Meng Han, Yan, Shao Xiao, Wu, Jing Qin, Soares, Jair C., De Yang, Fu, Zhang, Xiang Yang
• Format: Article
• Language: English
• Subjects: Animals; Antioxidants - pharmacology; BDNF; Brain-Derived Neurotrophic Factor - analysis; Corpus Striatum - chemistry; Disease Models, Animal; Extract of Ginkgo biloba; Ginkgo biloba; Haloperidol - pharmacology; Male; Mastication - drug effects; Plant Extracts - pharmacology; Plant Extracts - therapeutic use; Rats; Rats, Sprague-Dawley; Substantia Nigra - chemistry; Tardive dyskinesia; Tardive Dyskinesia - drug therapy; Tardive Dyskinesia - metabolism; Vacuous chewing movements; Vitamin E - pharmacology; Vitamin E - therapeutic use
• ISSN: 0091-3057; 1873-5177
• DOI: 10.1016/j.pbb.2016.06.003

Neurodegeneration may be involved in the development of tardive dyskinesia (TD), and low levels of brain-derived neurotrophic factor (BDNF) may play a role. Ginkgo biloba (EGb761), a potent antioxidant, may have neuroprotective effects. We hypothesized that there would be decreased BDNF expression in TD, but that treatment with EGb761 would increase BDNF expression and reduce TD manifestations in a rat model. Forty rats were treated with haloperidol (2mg/kg/day via intraperitoneal injections) for 5weeks. EGb761 (50mg/kg/day) and vitamin E (20mg/kg/day) were then administered by oral gavage for another 5weeks, and we compared the effects of treatment with EGb761 or vitamin E on haloperidol-induced vacuous chewing movements (VCMs) and BDNF expression in four brain regions: prefrontal cortex (PFC), striatum (ST), substantia nigra (SNR), and globus pallidus (GP). Our results showed that haloperidol administration led to a progressive increase in VCMs, but both EGb761 and vitamin E significantly decreased VCMs. Haloperidol also decreased BDNF expression in all four brain regions, but both EGb761 and vitamin E administration significantly increased BDNF expression. Our results showed that both EGb761 and VE treatments exerted similar positive effects in a rat model of TD and increased BDNF expression levels in the four tested brain regions, suggesting that both EGb761 and vitamin E improve TD symptoms, possibly by enhancing BDNF in the brain and/or via their free radical-scavenging actions. •The effects of EGb761 and vitamin E on TD and BDNF expression in brain regions were compared.•Both EGb761 and vitamin E significantly decreased the TD severity.•Both EGb761 and vitamin E significantly reversed the decreased BDNF in all studied brain regions.•Both EGb761 and vitamin E reduce TD symptoms, possibly via their effects on BDNF signaling.