Publication:
Melatonin attenuates methamphetamine-induced inhibition of neurogenesis in the adult mouse hippocampus: An in vivo study

2
0

Issued Date

2015

Resource Type

Article

File Type

application/pdf

ISSN

3043940

DOI

10.1016/j.neulet.2015.09.011

Other identifier(s)

2-s2.0-84941927186

Rights Holder(s)

มหาวิทยาลัยศรีนครินทรวิโรฒ

Bibliographic Citation

Neuroscience Letters. Vol 606, (2015), p.209-214

Suggested Citation

Singhakumar R., Boontem P., Ekthuwapranee K., Sotthibundhu A., Mukda S., Chetsawang B., Govitrapong P. Melatonin attenuates methamphetamine-induced inhibition of neurogenesis in the adult mouse hippocampus: An in vivo study. Neuroscience Letters. Vol 606, (2015), p.209-214. doi:10.1016/j.neulet.2015.09.011 Retrieved from: https://hdl.handle.net/20.500.14740/6046

Title

Melatonin attenuates methamphetamine-induced inhibition of neurogenesis in the adult mouse hippocampus: An in vivo study

Author(s)

Singhakumar R.
 Boontem P.
 Ekthuwapranee K.
 Sotthibundhu A.
 Mukda S.
 Chetsawang B.
 Govitrapong P.

Abstract

Methamphetamine (METH), a highly addictive psychostimulant drug, is known to exert neurotoxic effects to the dopaminergic neural system. Long-term METH administration impairs brain functions such as cognition, learning and memory. Newly born neurons in the dentate gyrus of the hippocampus play an important role in spatial learning and memory. Previous in vitro studies have shown that METH inhibits cell proliferation and neurogenesis in the hippocampus. On the other hand, melatonin, a major indole secreted by the pineal gland, enhances neurogenesis in both the subventricular zone and dentate gyrus. In this study, adult C57BL/6 mice were used to study the beneficial effects of melatonin on METH-induced alterations in neurogenesis and post-synaptic proteins related to learning and memory functions in the hippocampus. The results showed that METH caused a decrease in neuronal phenotypes as determined by the expressions of nestin, doublecortin (DCX) and beta-III tubulin while causing an increase in glial fibrillary acidic protein (GFAP) expression. Moreover, METH inhibited mitogen-activated protein kinase (MAPK) signaling activity and altered expression of the N-methyl-. d-aspartate (NMDA) receptor subunits NR2A and NR2B as well as calcium/calmodulin-dependent protein kinase II (CaMKII). These effects could be attenuated by melatonin pretreatment. In conclusion, melatonin prevented the METH-induced reduction in neurogenesis, increase in astrogliogenesis and alteration of NMDA receptor subunit expression. These findings may indicate the beneficial effects of melatonin on the impairment of learning and memory caused by METH. © 2015 Elsevier Ireland Ltd.

Subject(s)

Beta tubulin
 Calcium calmodulin dependent protein kinase II
 Doublecortin
 Glial fibrillary acidic protein
 Melatonin
 Methamphetamine
 Mitogen activated protein kinase
 N methyl dextro aspartic acid receptor
 Nestin
 Receptor subunit
 Central stimulant agent
 Melatonin
 Methamphetamine
 N methyl dextro aspartic acid receptor
 Protein subunit
 Animal experiment
 Animal tissue
 Article
 Controlled study
 Dentate gyrus
 Enzyme induction
 Hippocampus
 In vivo study
 Learning
 Male
 Memory
 Mouse
 Nervous system development
 Nonhuman
 Priority journal
 Protein expression
 Signal transduction
 Subventricular zone
 Animal
 C57BL mouse
 Cell differentiation
 Cell proliferation
 Drug effects
 Hippocampus
 Metabolism
 Nerve cell
 Nervous system development
 Neural stem cell
 Pathology
 Protein subunit
 Animals
 Cell Differentiation
 Cell Proliferation
 Central Nervous System Stimulants
 Hippocampus
 Male
 MAP Kinase Signaling System
 Melatonin
 Methamphetamine
 Mice, Inbred C57BL
 Neural Stem Cells
 Neurogenesis
 Neurons
 Protein Subunits
 Receptors, N-Methyl-D-Aspartate

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URI

https://hdl.handle.net/20.500.14740/6046

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Scopus: Year 1983-2021

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