Environmental enrichment improves long-term memory impairment and aberrant synaptic plasticity by BDNF/TrkB signaling in nerve-injured mice. (16th February 2019)

• Record Type: Journal Article
• Authors: Wang, Xing-Ming; Pan, Wei; Xu, Ning; Zhou, Zhi-Qiang; Zhang, Guang-Fen; Shen, Jin-Chun
• Is Part Of: Neuroscience letters. Volume 694(2019)
• Page Start: 93
• Page End: 98
• Publication Date: 2019-02-16
• Subjects: Nerve injury -- Memory -- Environmental enrichment -- Brain-derived neurotrophic factor; Neurology -- Periodicals; Neurology -- Periodicals; Research -- Periodicals; Neurologie -- Périodiques; Neuroanatomie -- Périodiques; Neuropharmacologie -- Périodiques; Neurophysiologie -- Périodiques; Neurology; Periodicals; Electronic journals; 617.48
• DOI: 10.1016/j.neulet.2018.11.049
• Languages: English
• ISSNs: 0304-3940

Abstract

Highlights: EE improved pain threshold reduction, long-term memory and synaptic plasticity deficits in nerve-injured mice. EE's effects on long-term memory and synaptic plasticity deficits may be reversed by TrkB antagonist in nerve imjured mice. EE improved long-term memory and synaptic plasticity deficits via BDNF / TrkB signaling in nerve-injured mice. Abstract: Nerve injury can induce memory impairment in mice. The aim of this research is to study the effect of environmental enrichment (EE) on long-term memory impairment in nerve-injured mice and the underlying mechanisms. Adult male C57BL/6 mice were received sham or chronic constriction injury (CCI) operation and reared in a standard environment (SE) or EE for 4 weeks after the operation. The pain threshold, long-term memory, expression of brain-derived neurotrophic factor (BDNF) and synaptic plasticity in hippocampus were determined. The results showed that CCI can induce the reduction in the mechanical and thermal pain thresholds, which were accompanied by long-term memory deficits in mice. CCI also induced the reduction of BDNF expression and synaptic plasticity impairments in the hippocampus, as represented by the dendritic spine density and postsynaptic density protein (PSD)-95 reduction, and long-term potential (LTP) dysfunction. Notably, EE can ameliorate the pain threshold and BDNF reduction, long-term memory deficits, and synaptic plasticity impairments in nerve-injured mice. However, the tropomyosin receptor kinase (Trk) B antagonist, ANA-12, blocked the EE-induced improvement in the long-term memory and synaptic plasticity impairment in nerve-injured mice. In conclusion, EE improved the pain threshold reduction, long-term memory and synaptic plasticity deficits in nerve-injured mice; BDNF / Trk B signaling may contribute to the relief of long-term memory and synaptic plasticity deficits induced by EE in nerve-injured mice.