PMID- 30605763
OWN - NLM
STAT- MEDLINE
DCOM- 20200109
LR  - 20200109
IS  - 1872-9711 (Electronic)
IS  - 0161-813X (Linking)
VI  - 71
DP  - 2019 Mar
TI  - Mechanistic comparison between MPTP and rotenone neurotoxicity in mice.
PG  - 113-121
LID - S0161-813X(18)30397-8 [pii]
LID - 10.1016/j.neuro.2018.12.009 [doi]
AB  - Animal models for Parkinson's disease (PD) are very useful in understanding the 
      pathogenesis of PD and screening for new therapeutic approaches. 
      1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine (MPTP) and rotenone are common 
      neurotoxins used for the development of experimental PD models, and both inhibit 
      complex I of mitochondria; this is thought to be an instrumental mechanism for 
      dopaminergic neurodegeneration in PD. In this study, we treated mice with MPTP 
      (30 mg/kg/day) or rotenone (2.5 mg/kg/day) for 1 week and compared the neurotoxic 
      effects of these toxins. MPTP clearly produced dopaminergic lesions in both the 
      substantia nigra and the striatum as shown by loss of dopaminergic neurons, 
      depletion of striatal dopamine, activation of glial cells in the nigrostriatal 
      pathway and behavioral impairment. In contrast, rotenone treatment did not show 
      any significant neuronal injury in the nigrostriatal pathway, but it caused 
      neurodegeneration and glial activation only in the hippocampus. MPTP showed no 
      such deleterious effects in the hippocampus suggesting the higher susceptibility 
      of the hippocampus to rotenone than to MPTP. Interestingly, rotenone caused 
      upregulation of the neurotrophic factors and their downstream PI3K-Akt pathway 
      along with adenosine monophosphate-activated protein kinase (AMPK) activation. 
      These results suggest that MPTP-induced dopaminergic neurotoxicity is more acute 
      and specific in comparison to rotenone toxicity, and compensatory brain-derived 
      neurotrophic factor (BDNF) induction and AMPK activation in the rotenone-treated 
      brain might suppress the neuronal injury.
CI  - Copyright (c) 2019 Elsevier B.V. All rights reserved.
FAU - Bhurtel, Sunil
AU  - Bhurtel S
AD  - Yeungnam University, 280 Daehak-Ro, Gyeongsan, Gyeongbuk, 38541, Republic of 
      Korea. Electronic address: bhurtelsunil11@gmail.com.
FAU - Katila, Nikita
AU  - Katila N
AD  - Yeungnam University, 280 Daehak-Ro, Gyeongsan, Gyeongbuk, 38541, Republic of 
      Korea. Electronic address: nikitakatila28@gmail.com.
FAU - Srivastav, Sunil
AU  - Srivastav S
AD  - Yeungnam University, 280 Daehak-Ro, Gyeongsan, Gyeongbuk, 38541, Republic of 
      Korea. Electronic address: sunsri2003@hotmail.com.
FAU - Neupane, Sabita
AU  - Neupane S
AD  - Yeungnam University, 280 Daehak-Ro, Gyeongsan, Gyeongbuk, 38541, Republic of 
      Korea. Electronic address: sabita_neupane@hotmail.com.
FAU - Choi, Dong-Young
AU  - Choi DY
AD  - Yeungnam University, 280 Daehak-Ro, Gyeongsan, Gyeongbuk, 38541, Republic of 
      Korea. Electronic address: dychoi@yu.ac.kr.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20181231
PL  - Netherlands
TA  - Neurotoxicology
JT  - Neurotoxicology
JID - 7905589
RN  - 03L9OT429T (Rotenone)
RN  - 102-32-9 (3,4-Dihydroxyphenylacetic Acid)
RN  - VTD58H1Z2X (Dopamine)
SB  - IM
MH  - 3,4-Dihydroxyphenylacetic Acid/metabolism
MH  - Animals
MH  - Astrocytes/drug effects/metabolism
MH  - Brain/*drug effects/metabolism/pathology
MH  - Dopamine/metabolism
MH  - MPTP Poisoning/*metabolism/*pathology
MH  - Male
MH  - Mice, Inbred C57BL
MH  - Neurons/*drug effects/metabolism/pathology
MH  - Parkinsonian Disorders/chemically induced/*metabolism/*pathology
MH  - Rotenone/*toxicity
OTO - NOTNLM
OT  - MPTP
OT  - Neurotrophic factors
OT  - Parkinson's disease
OT  - Rotenone
EDAT- 2019/01/04 06:00
MHDA- 2020/01/10 06:00
CRDT- 2019/01/04 06:00
PHST- 2018/09/27 00:00 [received]
PHST- 2018/12/24 00:00 [revised]
PHST- 2018/12/28 00:00 [accepted]
PHST- 2019/01/04 06:00 [pubmed]
PHST- 2020/01/10 06:00 [medline]
PHST- 2019/01/04 06:00 [entrez]
AID - S0161-813X(18)30397-8 [pii]
AID - 10.1016/j.neuro.2018.12.009 [doi]
PST - ppublish
SO  - Neurotoxicology. 2019 Mar;71:113-121. doi: 10.1016/j.neuro.2018.12.009. Epub 2018 
      Dec 31.