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Learning and Long-term Memory

開催日 2014/9/13
時間 14:00 - 15:00
会場 Poster / Exhibition(Event Hall B)

Impaired spatial memory associated with nmda receptor alterations in hippocampus of rats prenatally exposed to lambda-cyhalothrin

  • P3-222
  • Yogesh K Dhuriya:1 Rajendra Ku Shukla:1 Pranay Srivastava:1 Lalit Prata Chandravanshi:1 Vinay Kumar Khanna:1 
  • 1:Indian Institute of Toxicology Research, India 

Background:Exposure to Lambda-cyhalothrin (LCT), a new generation type II synthetic pyrethroid is significantly
enhanced due to its extensive applications and associated with neurobehavioral alterations in childrenâ€TMs.
Purpose:The present study has been carried out to investigate the effect of LCT on the brain glutamatergic functions in
developing rats and assess whether these changes are transient or persistent. Methods:Pregnant rats were exposed to
LCT (0.5mg/kg,1mg/kg or 3mg/kg body weight, p.o) from GD6-GD21.The spatial memory was assessed by Y-MAZE
and NMDA receptor binding was carried out by radioligand binding assay. mRNA levels of NMDA receptor subunits
were determined by RT-PCR and expression of apoptotic markers were assessed by western blotting. Assay of MMP,
enzyme complexes associated with the energy metabolism and generation of ROS in mitochondria was carried out in
hippocampus on postnatal day (PD) 22 & 45. Results:Prenatal exposure to LCT affect the spatial memory associated
with decrease in binding of NMDA receptors and mRNA levels of NMDA subunits in hippocampus on PD22. Enhanced
generation of ROS associated with decrease in the membrane potential (MMP) and activity of mitochondrial complexes
was distinct in rats on PD22. Alteration in the expression of apoptotic proteins in hippocampus were also observed.
While the intensity of changes was more marked at higher dose, a trend of recovery was observed at low doses on
PD45. Conclusion:The results exhibit that prenatal exposure to LCT impairs spatial memory by affecting the
hippocampal glutamatergic system. Interestingly, enhanced ROS generation and mitochondrial dysfunctions appear to
be associated in glutamatergic alterations.

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