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Published on: November 20, 2015
Prenatal exposure to lambda-cyhalothrin impairs memory in developing rats: Role of NMDA receptor induced
Yogesh K Dhuriya1, Pranay Srivastava2, Rajendra K Shukla2
1Developmental Toxicology Laboratory, Systems Toxicology and Health Risk Assessment Group, CSIR-Indian Institute of Toxicology Research (CSIR-IITR), Vishvigyan Bhawan, 31, Mahatma Gandhi Marg, Lucknow - 226 001, Uttar Pradesh, India; Academy of Scientific and Innovative Research (AcSIR), Lucknow Campus, India.
Insights
Prenatal exposure to lambda-cyhalothrin (LCT) in rats disrupts NMDA receptors and synaptic plasticity, impairing learning and memory. Effects persisted at high doses but showed recovery trends at moderate doses.
Area of Science:
- Neuroscience
- Developmental Toxicology
- Neuropharmacology
Background:
- Prenatal exposure to environmental toxins can impact neurodevelopment.
- N-methyl-D-aspartate (NMDA) receptors are crucial for synaptic plasticity and cognitive function.
- Lambda-cyhalothrin (LCT) is a widely used insecticide with potential neurotoxic effects.
Purpose of the Study:
- To investigate the effects of prenatal LCT exposure on NMDA receptor integrity and postsynaptic signaling in developing rat hippocampus.
- To assess the impact of LCT exposure on learning and memory in young rats.
Main Methods:
- Rats were exposed prenatally to varying doses of LCT (0.5, 1, and 3 mg/kg).
- NMDA receptor binding, mRNA, and protein expression (NR1, NR2A, NR2B) were analyzed.
- Expression of synaptic plasticity regulators (positive and negative) and neurobehavioral tests were performed.
Main Results:
- Prenatal LCT exposure decreased NMDA receptor binding and expression of NR1 and NR2B subunits.
- LCT altered the expression of synaptic plasticity regulators, decreasing positive ones (PSD95, pERK1/2, CaMKIIα, pCREB) and increasing negative ones (Cdk5, SynGAP).
- Impaired learning and memory were observed, with persistent deficits at high doses and partial recovery at moderate doses; low doses showed no effects.
Conclusions:
- Prenatal LCT exposure disrupts NMDA receptor function and postsynaptic signaling in the developing hippocampus.
- These alterations are associated with impaired learning and memory in developing rats.
- The neurotoxic effects are dose-dependent, with potential for recovery at lower exposure levels.
Abstract:
Effect of prenatal exposure to lambda-cyhalothrin (LCT) has been assessed on the integrity of NMDA receptors and associated post-synaptic signalling in hippocampus of developing rats. Decrease in the binding of [3H]-MK 801, known to label NMDA receptors was observed in hippocampus of rats prenatally exposed to LCT (1 and 3mg/kg body weight) on PD22, compared to controls. Consistent with this, decrease in the mRNA and protein expression of NR1 and NR2B subunits of NMDA receptors was evident in rats prenatally exposed to LCT (1 and 3mg/kg body weight) on PD22. There was no change in mRNA and protein expression of NR2A subunit of NMDA receptors. Prenatal exposure to LCT (1 and 3mg/kg body weight) decreased the expression of positive regulators (PSD95, pERK1/2, CaMKIIα & pCREB) and increased the expression of negative regulators (Cdk5 & SynGAP) associated with NMDA receptor dependent synaptic plasticity in hippocampus and impaired learning and memory of rats on PD22. The neurobehavioral changes continued to persist in rats exposed to LCT at high dose (3mg/kg body weight) while exhibited trend of recovery in those exposed at moderate dose (1mg/kg body weight) on PD45, compared to controls. No change in any of the neurobehavioral endpoint was observed in developing rats prenatally exposed to LCT at low dose (0.5mg/kg body weight) on PD22 and PD45. The results exhibit that alterations in NMDA receptors on prenatal exposure to LCT may affect postsynaptic signalling associated with impaired learning and memory in developing rats.
