PMID- 27058123
OWN - NLM
STAT- MEDLINE
DCOM- 20180321
LR  - 20211216
IS  - 1872-9711 (Electronic)
IS  - 0161-813X (Print)
IS  - 0161-813X (Linking)
VI  - 60
DP  - 2017 May
TI  - Developmental pyrethroid exposure causes long-term decreases of neuronal sodium 
      channel expression.
PG  - 274-279
LID - S0161-813X(16)30047-X [pii]
LID - 10.1016/j.neuro.2016.04.002 [doi]
AB  - Pyrethroid insecticide use has increased over recent years because of their low 
      to moderate acute toxicity in mammals. However, there is increasing concern over 
      the potential detrimental effects of pyrethroids on developing animals. Most 
      recently, we have shown that developmental exposure to deltamethrin results in 
      long-term neurobehavioral effects. Pyrethroids exert their toxicity by acting on 
      the voltage-gated sodium channel (Na(v)), delaying channel inactivation and 
      causing hyperexcitability in the nervous system. Previous in vitro studies found 
      that exposure to agents that increase Na(+) influx, including deltamethrin 
      decreased Na(v) mRNA expression. However, it is unknown whether this occurs in 
      vivo. To determine whether developmental pyrethroid exposure decreases Na(v) mRNA 
      expression, pregnant mice were exposed to the pyrethroid deltamethrin (0 or 
      3mg/kg) every three days throughout gestation and lactation. Na(v) mRNA 
      expression was measured in the striatum and cortex of the offspring at 10-11 
      months of age, a time at which behavioral abnormalities were still observed. 
      Developmental exposure to deltamethrin decreased expression of Na(v) mRNA in a 
      region- and isoform-specific fashion by 24-50%. Deltamethrin exposure also 
      resulted in the persistent down-regulation of brain-derived neurotrophic factor 
      (Bdnf) in the striatum by 66% but not in the cortex, suggesting a plausible 
      mechanism for some of the associated behavioral effects observed previously. 
      Taken together these data suggest that developmental deltamethrin exposure 
      results in persistent deficits in Na(v) and BDNF mRNA expression that may 
      contribute to long-term behavioral deficits.
CI  - Copyright (c) 2016. Published by Elsevier B.V.
FAU - Magby, Jason P
AU  - Magby JP
AD  - Environmental and Occupational Health Sciences Institute and Department of 
      Environmental and Occupational Medicine, Robert Wood Johnson Medical School, 
      Rutgers University, Piscataway, NJ 08854, USA.
FAU - Richardson, Jason R
AU  - Richardson JR
AD  - Environmental and Occupational Health Sciences Institute and Department of 
      Environmental and Occupational Medicine, Robert Wood Johnson Medical School, 
      Rutgers University, Piscataway, NJ 08854, USA; Northeast Ohio Medical University 
      Department of Pharmaceutical Sciences, Rootstown, OH 44272, USA. Electronic 
      address: jrichardson@neomed.edu.
LA  - eng
GR  - P30 ES005022/ES/NIEHS NIH HHS/United States
GR  - R01 ES015991/ES/NIEHS NIH HHS/United States
GR  - R21 ES013828/ES/NIEHS NIH HHS/United States
PT  - Journal Article
DEP - 20160404
PL  - Netherlands
TA  - Neurotoxicology
JT  - Neurotoxicology
JID - 7905589
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Insecticides)
RN  - 0 (Nitriles)
RN  - 0 (Pyrethrins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Voltage-Gated Sodium Channels)
RN  - 2JTS8R821G (decamethrin)
SB  - IM
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/metabolism
MH  - Cerebral Cortex/*drug effects/growth & development/metabolism
MH  - Corpus Striatum/*drug effects/growth & development/metabolism
MH  - Female
MH  - Insecticides/*toxicity
MH  - Male
MH  - Mice, Inbred C57BL
MH  - Neurons/*drug effects/metabolism
MH  - Nitriles/*toxicity
MH  - Pregnancy
MH  - Prenatal Exposure Delayed Effects/*metabolism
MH  - Pyrethrins/*toxicity
MH  - RNA, Messenger/metabolism
MH  - Voltage-Gated Sodium Channels/*metabolism
PMC - PMC8669832
MID - NIHMS1592996
OTO - NOTNLM
OT  - BDNF
OT  - Deltamethrin
OT  - Neurodevelopmental
OT  - Pyrethroid
OT  - Sodium channel
COIS- Conflict of interest The authors declare they have no conflict of interest.
EDAT- 2016/04/09 06:00
MHDA- 2018/03/22 06:00
PMCR- 2021/12/14
CRDT- 2016/04/09 06:00
PHST- 2015/12/15 00:00 [received]
PHST- 2016/03/24 00:00 [revised]
PHST- 2016/04/01 00:00 [accepted]
PHST- 2016/04/09 06:00 [pubmed]
PHST- 2018/03/22 06:00 [medline]
PHST- 2016/04/09 06:00 [entrez]
PHST- 2021/12/14 00:00 [pmc-release]
AID - S0161-813X(16)30047-X [pii]
AID - 10.1016/j.neuro.2016.04.002 [doi]
PST - ppublish
SO  - Neurotoxicology. 2017 May;60:274-279. doi: 10.1016/j.neuro.2016.04.002. Epub 2016 
      Apr 4.