Publication: Melatonin reverts methamphetamine-induced learning and memory impairments and hippocampal alterations in mice
Issued Date
2021-01-15
Resource Type
ISSN
18790631
00243205
00243205
Other identifier(s)
2-s2.0-85097434985
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Mahidol University
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SCOPUS
Bibliographic Citation
Life Sciences. Vol.265, (2021)
Suggested Citation
Nisarath Veschsanit, Jenq Lin Yang, Sukonthar Ngampramuan, Kittikun Viwatpinyo, Jitrapa Pinyomahakul, Thit Lwin, Pongrung Chancharoen, Saowalak Rungruang, Piyarat Govitrapong, Sujira Mukda Melatonin reverts methamphetamine-induced learning and memory impairments and hippocampal alterations in mice. Life Sciences. Vol.265, (2021). doi:10.1016/j.lfs.2020.118844 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/76305
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Title
Melatonin reverts methamphetamine-induced learning and memory impairments and hippocampal alterations in mice
Abstract
Aims: Methamphetamine (METH) has become a major public health problem because of its abuse and profound neurotoxic effects, causing alterations in brain structure and function, and impairing cognitive functions, including attention, decision making, emotional memory, and working memory. This study aimed to determine whether melatonin (MEL), the circadian-control hormone, which has roles beyond circadian rhythm regulation, could restore METH-induced cognitive and neuronal impairment. Main methods: Mice were treated with either METH (1 mg/kg) or saline for 7 days, followed by MEL (10 mg/kg) or saline for another 14 days. The Morris water maze (MWM) test was performed one day after the last saline or MEL injection. The hippocampal neuronal density, synaptic density, and receptors involved in learning and memory, along with downstream signaling molecules (NMDA receptor subunits GluN2A, GluN2B, and CaMKII) were investigated by immunoblotting. Key findings: METH administration significantly extended escape latency in learning phase and reduced the number of target crossings in memory test-phase as well as decreased the expression of BDNF, NMDA receptors, TrkB receptors, CaMKII, βIII tubulin, and synaptophysin. MEL treatment significantly ameliorated METH-induced increased escape latency, decreased the number of target crossings and decreased expression of BDNF, NMDA receptors, TrkB receptors, CaMKII, βIII tubulin and synaptophysin. Significance: METH administration impairs learning and memory in mice, and MEL administration restores METH-induced neuronal impairments which is probably through the changes in BDNF, NMDA receptors, TrkB receptors, CaMKII, βIII tubulin and synaptophysin. Therefore, MEL is potentially an innovative and promising treatment for learning and memory impairment of humans.