Abstract
Cognitive flexibility is a crucial ability in humans that can be affected by chronic methamphetamine (METH) addiction. The present study aimed to elucidate the mechanisms underlying cognitive impairment in mice chronically administered METH via an oral self-administration method. Further, the effect of melatonin treatment on recovery of METH-induced cognitive impairment was also investigated. Cognitive performance of the mice was assessed using an attentional set shift task (ASST), and possible underlying neurotoxic mechanisms were investigated by proteomic and western blot analysis of the prefrontal cortex (PFC). The results showed that mice-administered METH for 21 consecutive days exhibited poor cognitive performance compared to controls. Cognitive deficit in mice partly recovered after METH withdrawal. In addition, mice treated with melatonin during METH withdrawal showed a higher cognitive recovery than vehicle-treated METH withdrawal mice. Proteomic and western blot analysis revealed that METH self-administration increased neurotoxic markers, including disruption to the regulation of mitochondrial function, mitophagy, and decreased synaptic plasticity. Treatment with melatonin during withdrawal restored METH-induced mitochondria and synaptic impairments. These findings suggest that METH-induced neurotoxicity partly depends on mitochondrial dysfunction leading to autophagy-dependent cell death and that the recovery of neurological impairments may be enhanced by melatonin treatment during the withdrawal period.
| Original language | English |
|---|---|
| Pages (from-to) | 3348-3359 |
| Number of pages | 12 |
| Journal | Journal of Proteome Research |
| Volume | 22 |
| Issue number | 10 |
| DOIs | |
| Publication status | Published - 6 Oct 2023 |
Bibliographical note
Copyright the Author(s) 2023. Version archived for private and non-commercial use with the permission of the author/s and according to publisher conditions. For further rights please contact the publisher.
Keywords
- cognitive function
- drug addiction
- melatonin
- methamphetamine
- mitochondria
- mitophagy
- neurodegeneration
- neuroplasticity
- neurotoxicity
- proteomics
Access to Document
10.1021/acs.jproteome.3c00502Licence: CC BY
Publisher version (open access)Final published version, 6.1 MBLicence: CC BY
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Polvat, T., Prasertp*rn, T., Na Nakorn, P., Pannengpetch, S., Suwanjang, W., Panmanee, J., Ngampramuan, S., Cornish, J. L., & Chetsawang, B. (2023). Proteomic analysis reveals the neurotoxic effects of chronic methamphetamine self-administration-induced cognitive impairments and the role of melatonin-enhanced restorative process during methamphetamine withdrawal. Journal of Proteome Research, 22(10), 3348-3359. https://doi.org/10.1021/acs.jproteome.3c00502
Polvat, Tanthai ; Prasertp*rn, Tanya ; Na Nakorn, Piyada et al. / Proteomic analysis reveals the neurotoxic effects of chronic methamphetamine self-administration-induced cognitive impairments and the role of melatonin-enhanced restorative process during methamphetamine withdrawal. In: Journal of Proteome Research. 2023 ; Vol. 22, No. 10. pp. 3348-3359.
@article{0957db303a0e4d03854fe92c777475c7,
title = "Proteomic analysis reveals the neurotoxic effects of chronic methamphetamine self-administration-induced cognitive impairments and the role of melatonin-enhanced restorative process during methamphetamine withdrawal",
abstract = "Cognitive flexibility is a crucial ability in humans that can be affected by chronic methamphetamine (METH) addiction. The present study aimed to elucidate the mechanisms underlying cognitive impairment in mice chronically administered METH via an oral self-administration method. Further, the effect of melatonin treatment on recovery of METH-induced cognitive impairment was also investigated. Cognitive performance of the mice was assessed using an attentional set shift task (ASST), and possible underlying neurotoxic mechanisms were investigated by proteomic and western blot analysis of the prefrontal cortex (PFC). The results showed that mice-administered METH for 21 consecutive days exhibited poor cognitive performance compared to controls. Cognitive deficit in mice partly recovered after METH withdrawal. In addition, mice treated with melatonin during METH withdrawal showed a higher cognitive recovery than vehicle-treated METH withdrawal mice. Proteomic and western blot analysis revealed that METH self-administration increased neurotoxic markers, including disruption to the regulation of mitochondrial function, mitophagy, and decreased synaptic plasticity. Treatment with melatonin during withdrawal restored METH-induced mitochondria and synaptic impairments. These findings suggest that METH-induced neurotoxicity partly depends on mitochondrial dysfunction leading to autophagy-dependent cell death and that the recovery of neurological impairments may be enhanced by melatonin treatment during the withdrawal period.",
keywords = "cognitive function, drug addiction, melatonin, methamphetamine, mitochondria, mitophagy, neurodegeneration, neuroplasticity, neurotoxicity, proteomics",
author = "Tanthai Polvat and Tanya Prasertp*rn and {Na Nakorn}, Piyada and Supitcha Pannengpetch and Wilasinee Suwanjang and Jirap*rn Panmanee and Sukhonthar Ngampramuan and Cornish, {Jennifer L.} and Banthit Chetsawang",
note = "Copyright the Author(s) 2023. Version archived for private and non-commercial use with the permission of the author/s and according to publisher conditions. For further rights please contact the publisher.",
year = "2023",
month = oct,
day = "6",
doi = "10.1021/acs.jproteome.3c00502",
language = "English",
volume = "22",
pages = "3348--3359",
journal = "Journal of Proteome Research",
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Polvat, T, Prasertp*rn, T, Na Nakorn, P, Pannengpetch, S, Suwanjang, W, Panmanee, J, Ngampramuan, S, Cornish, JL & Chetsawang, B 2023, 'Proteomic analysis reveals the neurotoxic effects of chronic methamphetamine self-administration-induced cognitive impairments and the role of melatonin-enhanced restorative process during methamphetamine withdrawal', Journal of Proteome Research, vol. 22, no. 10, pp. 3348-3359. https://doi.org/10.1021/acs.jproteome.3c00502
Proteomic analysis reveals the neurotoxic effects of chronic methamphetamine self-administration-induced cognitive impairments and the role of melatonin-enhanced restorative process during methamphetamine withdrawal. / Polvat, Tanthai; Prasertp*rn, Tanya; Na Nakorn, Piyada et al.
In: Journal of Proteome Research, Vol. 22, No. 10, 06.10.2023, p. 3348-3359.
Research output: Contribution to journal › Article › peer-review
TY - JOUR
T1 - Proteomic analysis reveals the neurotoxic effects of chronic methamphetamine self-administration-induced cognitive impairments and the role of melatonin-enhanced restorative process during methamphetamine withdrawal
AU - Polvat, Tanthai
AU - Prasertp*rn, Tanya
AU - Na Nakorn, Piyada
AU - Pannengpetch, Supitcha
AU - Suwanjang, Wilasinee
AU - Panmanee, Jirap*rn
AU - Ngampramuan, Sukhonthar
AU - Cornish, Jennifer L.
AU - Chetsawang, Banthit
N1 - Copyright the Author(s) 2023. Version archived for private and non-commercial use with the permission of the author/s and according to publisher conditions. For further rights please contact the publisher.
PY - 2023/10/6
Y1 - 2023/10/6
N2 - Cognitive flexibility is a crucial ability in humans that can be affected by chronic methamphetamine (METH) addiction. The present study aimed to elucidate the mechanisms underlying cognitive impairment in mice chronically administered METH via an oral self-administration method. Further, the effect of melatonin treatment on recovery of METH-induced cognitive impairment was also investigated. Cognitive performance of the mice was assessed using an attentional set shift task (ASST), and possible underlying neurotoxic mechanisms were investigated by proteomic and western blot analysis of the prefrontal cortex (PFC). The results showed that mice-administered METH for 21 consecutive days exhibited poor cognitive performance compared to controls. Cognitive deficit in mice partly recovered after METH withdrawal. In addition, mice treated with melatonin during METH withdrawal showed a higher cognitive recovery than vehicle-treated METH withdrawal mice. Proteomic and western blot analysis revealed that METH self-administration increased neurotoxic markers, including disruption to the regulation of mitochondrial function, mitophagy, and decreased synaptic plasticity. Treatment with melatonin during withdrawal restored METH-induced mitochondria and synaptic impairments. These findings suggest that METH-induced neurotoxicity partly depends on mitochondrial dysfunction leading to autophagy-dependent cell death and that the recovery of neurological impairments may be enhanced by melatonin treatment during the withdrawal period.
AB - Cognitive flexibility is a crucial ability in humans that can be affected by chronic methamphetamine (METH) addiction. The present study aimed to elucidate the mechanisms underlying cognitive impairment in mice chronically administered METH via an oral self-administration method. Further, the effect of melatonin treatment on recovery of METH-induced cognitive impairment was also investigated. Cognitive performance of the mice was assessed using an attentional set shift task (ASST), and possible underlying neurotoxic mechanisms were investigated by proteomic and western blot analysis of the prefrontal cortex (PFC). The results showed that mice-administered METH for 21 consecutive days exhibited poor cognitive performance compared to controls. Cognitive deficit in mice partly recovered after METH withdrawal. In addition, mice treated with melatonin during METH withdrawal showed a higher cognitive recovery than vehicle-treated METH withdrawal mice. Proteomic and western blot analysis revealed that METH self-administration increased neurotoxic markers, including disruption to the regulation of mitochondrial function, mitophagy, and decreased synaptic plasticity. Treatment with melatonin during withdrawal restored METH-induced mitochondria and synaptic impairments. These findings suggest that METH-induced neurotoxicity partly depends on mitochondrial dysfunction leading to autophagy-dependent cell death and that the recovery of neurological impairments may be enhanced by melatonin treatment during the withdrawal period.
KW - cognitive function
KW - drug addiction
KW - melatonin
KW - methamphetamine
KW - mitochondria
KW - mitophagy
KW - neurodegeneration
KW - neuroplasticity
KW - neurotoxicity
KW - proteomics
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M3 - Article
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SN - 1535-3893
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Polvat T, Prasertp*rn T, Na Nakorn P, Pannengpetch S, Suwanjang W, Panmanee J et al. Proteomic analysis reveals the neurotoxic effects of chronic methamphetamine self-administration-induced cognitive impairments and the role of melatonin-enhanced restorative process during methamphetamine withdrawal. Journal of Proteome Research. 2023 Oct 6;22(10):3348-3359. doi: 10.1021/acs.jproteome.3c00502
