Please use this identifier to cite or link to this item: https://ir.swu.ac.th/jspui/handle/123456789/13643
Title: Neuroprotective effects of melatonin on amphetamine-induced dopaminergic fiber degeneration in the hippocampus of postnatal rats
Authors: Leeboonngam T.
Pramong R.
Sae-ung K.
Govitrapong P.
Phansuwan-Pujito P.
Keywords: 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
Issue Date: 2018
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
URI: https://ir.swu.ac.th/jspui/handle/123456789/13643
https://www.scopus.com/inward/record.uri?eid=2-s2.0-85037377780&doi=10.1111%2fjpi.12456&partnerID=40&md5=769236511700900a2ba6d2418e3f3846
ISSN: 7423098
Appears in Collections:Scopus 1983-2021

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