Research article summary (published 2 May 2009):

Melatonin attenuates methamphetamine-induced reduction of tyrosine hydroxylase, synaptophysin and growth-associated protein-43 levels in the neonatal rat brain.

Full Abstract

Methamphetamine (METH) is a most commonly abused drug which damages nerve terminals by causing formation of reactive oxygen species (ROS), apoptosis, and finally neuronal damage. Fetal exposure to neurotoxic METH causes significant behavioral effects. The developing fetus is substantially deficient in most antioxidative enzymes, and may therefore be at high risk from both endogenous and drug-enhanced oxidative stress. Little is known about the effects of METH on vesicular proteins such as synaptophysin and growth-associated protein 43 (GAP-43) in the immature brain. The present study attempted to investigate the effects of METH-induced neurotoxicity in the dopaminergic system of the neonatal rat brain. Neonatal rats were subcutaneously exposed to 5-10mg/kg METH daily from postnatal day 4-10 for 7 consecutive days. The results showed that tyrosine hydroxylase enzyme levels were significantly decreased in the dorsal striatum, prefrontal cortex, nucleus accumbens and substantia nigra, synaptophysin levels decreased in the striatum and prefrontal cortex and growth-associated protein-43 (GAP-43) levels significantly decreased in the nucleus accumbens of neonatal rats. Pretreatment with 2mg/kg melatonin 30 min prior to METH administration prevented METH-induced reduction in tyrosine hydroxylase, synaptophysin and growth-associated protein-43 protein levels in different brain regions. These results suggest that melatonin provides a protective effect against METH-induced nerve terminal degeneration in the immature rat brain probably via its antioxidant properties.

Author information

Author/s: Kaewsuk, Sukit (S); Sae-ung, Kwankanit (K); Phansuwan-Pujito, Pansiri (P); Govitrapong, Piyarat (P);

Affiliation: Neuro-Behavioral Biology Center, Institute of Science and Technology for Research and Development, Mahidol University, Salaya, Nakornpathom 73170, Thailand.

Journal and publication information

Publication Type: Journal Article; Research Support, Non-U.S. Gov't

Journal: Neurochemistry international (Neurochem Int), published in England. (Language: eng)

Reference: 2009-Nov; vol 55 (issue 6) : pp 397-405

Dates: Created 2009/07/17; Completed 2009/10/09;

PMID: 19409439, status: MEDLINE (last retrieval date: 10/9/2009, IMS Date: )

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

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MeSH headings (categories)

This article was linked to the MESH Headings shown below.

Amphetamine-Related Disorders - drug therapy; metabolism; physiopathology Animals Animals, Newborn Antioxidants - pharmacology Brain - drug effects; growth & development; metabolism Brain Chemistry - drug effects; physiology Central Nervous System Stimulants - adverse effects Dopamine - biosynthesis Down-Regulation - drug effects; physiology Drug Interactions - physiology Female GAP-43 Protein - drug effects; metabolism

GAP-43 Protein - drug effects; metabolism Melatonin - pharmacology Methamphetamine - antagonists & inhibitors; toxicity Neuroprotective Agents - pharmacology Pregnancy Prenatal Exposure Delayed Effects - drug therapy; metabolism; physiopathology Presynaptic Terminals - drug effects; metabolism; pathology Rats Rats, Wistar Synaptophysin - drug effects; metabolism Tyrosine 3-Monooxygenase - drug effects; metabolism Wallerian Degeneration - chemically induced; drug therapy; prevention & control

Associated Chemicals: Antioxidants (0) ; Central Nervous System Stimulants (0) ; GAP-43 Protein (0) ; Neuroprotective Agents (0) ; Synaptophysin (0) ; Methamphetamine (537-46-2) ; Melatonin (73-31-4) ; Tyrosine 3-Monooxygenase (EC 1.14.16.2)

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