PMID- 12111003
OWN - NLM
STAT- MEDLINE
DCOM- 20030326
LR  - 20131121
IS  - 0340-5761 (Print)
IS  - 0340-5761 (Linking)
VI  - 76
IP  - 7
DP  - 2002 Jul
TI  - Neonatal exposure of newborn mice to pyrethroid (permethrin) represses 
      activity-dependent c-fos mRNA expression in cerebellum.
PG  - 392-7
AB  - In a previous report, we demonstrated that the exposure of cultured mouse 
      cerebellar granule cells to permethrin, a type I pyrethroid insecticide, 
      repressed the induction of activity-dependent c- fos and brain-derived 
      neurotrophic factor (BDNF) gene expression, accompanying a decrease in Ca(2+) 
      influx into neurons. In addition, it has been suggested that some pyrethroids, 
      including permethrin, are endocrine-modulating chemicals and accumulate in human 
      breast milk. In this study, therefore, we investigated whether lactational 
      exposure of newborn mice to permethrin influenced c- fos, BDNF and beta-actin 
      gene expression in the developing neonatal cerebellum. In the cerebella of 
      control neonates, c- fos mRNA expression was characterized by a significant 
      increase in postnatal weeks 2 and 3, followed by a marked decrease. In the 
      cerebella of permethrin-treated neonates, the expression of c- fos mRNA was 
      dose-dependently repressed by cis-permethrin more effectively than by 
      trans-permethrin at postnatal week 3, without alterations in the body or 
      cerebellum weights of neonates. In the fourth and fifth week, however, c- fos 
      mRNA expression had decreased to the same level as that in the control and 
      permethrin-treated neonates. A decrease in BDNF mRNA expression tended to be 
      observed in the cerebella of newborn mice on exposure to permethrin. Thus, our 
      results indicate that the activity-dependent gene expressions in cerebellar 
      neuronal cells can be repressed by permethrin both in vitro and in vivo, and 
      suggest that lactational exposure to pyrethroids might affect the postnatal 
      development of the mammalian brain.
FAU - Imamura, Lisa
AU  - Imamura L
AD  - Core Research for Evolutional Science and Technology, Japan Science and 
      Technology Corporation, Shibuya 3-13-11, Tokyo 150-0002, Japan.
FAU - Hasegawa, Hiroshi
AU  - Hasegawa H
FAU - Kurashina, Kaori
AU  - Kurashina K
FAU - Matsuno, Tomoya
AU  - Matsuno T
FAU - Tsuda, Masaaki
AU  - Tsuda M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20020529
PL  - Germany
TA  - Arch Toxicol
JT  - Archives of toxicology
JID - 0417615
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Insecticides)
RN  - 0 (Proto-Oncogene Proteins c-fos)
RN  - 0 (RNA, Messenger)
RN  - 509F88P9SZ (Permethrin)
SB  - IM
MH  - Animals
MH  - Animals, Newborn
MH  - Blotting, Northern
MH  - Brain-Derived Neurotrophic Factor/biosynthesis/genetics
MH  - Cerebellum/*drug effects/metabolism
MH  - Chrysanthemum cinerariifolium
MH  - Female
MH  - Gene Expression/drug effects
MH  - Insecticides/*toxicity
MH  - Lactation/metabolism
MH  - Male
MH  - Maximum Tolerated Dose
MH  - Mice
MH  - Mice, Inbred ICR
MH  - Permethrin/*toxicity
MH  - Proto-Oncogene Proteins c-fos/*biosynthesis/genetics
MH  - RNA, Messenger/*biosynthesis
EDAT- 2002/07/12 10:00
MHDA- 2003/03/27 05:00
CRDT- 2002/07/12 10:00
PHST- 2001/12/10 00:00 [received]
PHST- 2002/04/18 00:00 [accepted]
PHST- 2002/07/12 10:00 [pubmed]
PHST- 2003/03/27 05:00 [medline]
PHST- 2002/07/12 10:00 [entrez]
AID - 10.1007/s00204-002-0358-2 [doi]
PST - ppublish
SO  - Arch Toxicol. 2002 Jul;76(7):392-7. doi: 10.1007/s00204-002-0358-2. Epub 2002 May 
      29.