Melatonin enhances the restoration of neurological impairments and cognitive deficits during drug withdrawal in methamphetamine-induced toxicity and endoplasmic reticulum stress in rats
Issued Date
2023-12-01
Resource Type
ISSN
0161813X
eISSN
18729711
Scopus ID
2-s2.0-85177747526
Pubmed ID
37979660
Journal Title
NeuroToxicology
Volume
99
Start Page
305
End Page
312
Rights Holder(s)
SCOPUS
Bibliographic Citation
NeuroToxicology Vol.99 (2023) , 305-312
Suggested Citation
Komlao P., Kraiwattanapirom N., Promyo K., Hein Z.M., Chetsawang B. Melatonin enhances the restoration of neurological impairments and cognitive deficits during drug withdrawal in methamphetamine-induced toxicity and endoplasmic reticulum stress in rats. NeuroToxicology Vol.99 (2023) , 305-312. 312. doi:10.1016/j.neuro.2023.11.006 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/91324
Title
Melatonin enhances the restoration of neurological impairments and cognitive deficits during drug withdrawal in methamphetamine-induced toxicity and endoplasmic reticulum stress in rats
Other Contributor(s)
Abstract
Methamphetamine (METH) is a psychostimulant with a very high addiction rate. Prolonged use of METH has been observed as one of the root causes of neurotoxicity. Melatonin (Mel) has been found to have a significant role in METH-induced neurotoxicity. This study aimed to investigate the restorative effect of Mel on behavioral flexibility in METH-induced cognitive deficits. Male Sprague-Dawley rats were randomly assigned to be intraperitoneally injected with saline (control) or Meth at 5 mg/kg for 7 consecutive days. Then, METH injection was withdrawn and rats in each group were subcutaneously injected with saline or Mel at 10 mg/kg for 14 consecutive days. The stereotypic behavioral test and attentional set-shifting task (ASST) were used to evaluate neurological functions and cognitive flexibility, respectively. Rats developed abnormal features of stereotyped behaviors and deficits in cognitive flexibility after 7 days of METH administration. However, post-treatment with Mel for 14 days after METH withdrawal dramatically ameliorated the neurological and cognitive deficits in METH-treated rats. Blood biomarkers indicated METH-induced systemic low-grade inflammation. Moreover, METH-induced endoplasmic reticulum (ER) stress in the prefrontal cortex was diminished by melatonin supplementation. These findings might reveal the therapeutic potential of Mel in METH toxicity-induced neurological and cognitive deficits.