Publication:
Neuroprotective effects of melatonin on amphetamine-induced dopaminergic fiber degeneration in the hippocampus of postnatal rats

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Issued Date

2018

Resource Type

Article

File Type

application/pdf

ISSN

7423098

DOI

10.1111/jpi.12456

Other identifier(s)

2-s2.0-85037377780

Rights Holder(s)

มหาวิทยาลัยศรีนครินทรวิโรฒ

Bibliographic Citation

Journal of Pineal Research. Vol 64, No.3 (2018)

Suggested Citation

Leeboonngam T., Pramong R., Sae-Ung K., Govitrapong P., Phansuwan-Pujito P. Neuroprotective effects of melatonin on amphetamine-induced dopaminergic fiber degeneration in the hippocampus of postnatal rats. Journal of Pineal Research. Vol 64, No.3 (2018). doi:10.1111/jpi.12456 Retrieved from: https://hdl.handle.net/20.500.14740/6062

Title

Neuroprotective effects of melatonin on amphetamine-induced dopaminergic fiber degeneration in the hippocampus of postnatal rats

Author(s)

Leeboonngam T.
 Pramong R.
 Sae-Ung K.
 Govitrapong P.
 Phansuwan-Pujito P.

Abstract

Chronic amphetamine (AMPH) abuse leads to damage of the hippocampus, the brain area associated with learning and memory process. Previous results have shown that AMPH-induced dopamine neurotransmitter release, reactive oxygen species formation, and degenerative protein aggregation lead to neuronal death. Melatonin, a powerful antioxidant, plays a role as a neuroprotective agent. The objective of this study was to investigate whether the protective effect of melatonin on AMPH-induced hippocampal damage in the postnatal rat acts through the dopaminergic pathway. Four-day-old postnatal rats were subcutaneously injected with 5-10 mg/kg AMPH and pretreated with 10 mg/kg melatonin prior to AMPH exposure for seven days. The results showed that melatonin decreased the AMPH-induced hippocampal neuronal degeneration in the dentate gyrus, CA1, and CA3. Melatonin attenuated the reduction in the expression of hippocampal synaptophysin, PSD-95, α-synuclein, and N-methyl-D-aspartate (NMDA) receptor protein and mRNA caused by AMPH. Melatonin attenuated the AMPH-induced reduction in dopamine transporter (DAT) protein expression in the hippocampus and the reduction in mRNA expression in the ventral tegmental area (VTA). Immunofluorescence demonstrated that melatonin not only prevented the AMPH-induced loss of DAT and NMDA receptor but also prevented AMPH-induced α-synuclein overexpression in the dentate gyrus, CA1, and CA3. Melatonin decreased the AMPH-induced reduction in the protein and mRNA of the NMDA receptor downstream signaling molecule, calcium/calmodulin-dependent protein kinase II (CaMKII), and the melatonin receptors (MT1 and MT2). This study showed that melatonin prevented AMPH-induced toxicity in the hippocampus of postnatal rats possibly via its antioxidative effect and mitochondrial protection. © 2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd

Subject(s)

Alpha synuclein
 Amphetamine
 Calcium calmodulin dependent protein kinase II
 Dopamine transporter
 Melatonin
 Melatonin 1 receptor
 Melatonin 2 receptor
 Messenger RNA
 N methyl dextro aspartic acid receptor
 SAP90/PSD95 associated protein
 Synaptophysin
 Amphetamine
 Central stimulant agent
 Melatonin
 Neuroprotective agent
 Animal experiment
 Animal model
 Animal tissue
 Article
 Controlled study
 Dentate gyrus
 Dopaminergic nerve cell
 Female
 Hippocampal CA1 region
 Hippocampal CA3 region
 Hippocampus
 Immunofluorescence
 Immunoreactivity
 Nerve fiber degeneration
 Neuroprotection
 Newborn
 Nonhuman
 Protein expression
 Rat
 Real time polymerase chain reaction
 Ventral tegmentum
 Western blotting
 Animal
 Chemically induced
 Dopaminergic nerve cell
 Drug effect
 Hippocampus
 Nerve degeneration
 Pathology
 Wistar rat
 Amphetamine
 Animals
 Central Nervous System Stimulants
 Dopaminergic Neurons
 Hippocampus
 Melatonin
 Nerve Degeneration
 Neuroprotective Agents
 Rats
 Rats, Wistar

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URI

https://hdl.handle.net/20.500.14740/6062

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Scopus: Year 1983-2021

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