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Lasting Increases in Neuronal Activity and Serotonergic Receptor Expression Following Gestational Chlorpyrifos
Jeffrey A Koenig1, Nathan Cramer1, Kara Kessler1
1Department of Neurobiology and UM-MIND, University of Maryland School of Medicine, Baltimore, Maryland 21201.
Gestational exposure to chlorpyrifos (CPF) insecticide increases spontaneous neuronal firing in rat brains. This neurotoxicity may underlie neurodevelopmental disorders like autism spectrum disorder.
Area of Science:
- Neuroscience
- Developmental Neuroscience
- Environmental Toxicology
Background:
- Perinatal exposure to chlorpyrifos (CPF) is linked to neurodevelopmental disorders.
- Previous studies show altered synaptic transmission and serotonin receptor binding post-CPF exposure.
- Functional brain alterations remain largely unknown.
Purpose of the Study:
- Investigate if gestational CPF exposure increases spontaneous firing of inhibitory interneurons.
- Determine if CPF exposure alters serotonin receptor expression in the developing brain.
Main Methods:
- Used a rat model for gestational CPF exposure.
- Employed ex vivo electrophysiology to assess neuronal firing in the somatosensory cortex.
- Utilized immunohistochemistry and RNAscope in situ hybridization to analyze neuronal activity and receptor expression.
Main Results:
- CPF-exposed offspring showed increased spontaneous neuronal firing in the somatosensory cortex.
- Fast-spiking parvalbumin (PV) interneurons were identified as a subset of hyperactive neurons.
- Increased expression of the 5-HT1B receptor was observed in PV neurons of male offspring.
Conclusions:
- Gestational CPF exposure may lead to persistent somatosensory cortex hyper-excitation.
- These neurophysiological changes could contribute to CPF-associated behavioral deficits.
- Findings offer insights into mechanisms underlying neurodevelopmental disorders linked to early-life insecticide exposure.
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