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Hippocampal Vulnerability to Environmental Pesticide Exposure

Award Number: R01ES038738
ORGANIZATION: NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 09/16/2026
PERIOD OF PERFORMANCE END DATE: 06/30/2031

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Hippocampal Vulnerability to Environmental Pesticide Exposure - ABSTRACT Epidemiological studies link early-life exposure to pesticides, including pyrethroids, with increased risk of neurodevelopmental disorders (NDDs) such as autism spectrum disorders (ASDs) and attention deficit hyperactivity disorder (ADHD). A growing body of evidence suggests that selective vulnerability of specific neuronal subtypes may underlie how these exposures contribute to NDD susceptibility. However, the specific neural cell types and brain regions most affected by pyrethroid exposure, and how this translates to functional circuit and behavioral disruption, remain largely unexplored. This study addresses that gap using deltamethrin (DM), a widely used pyrethroid pesticide that accumulates in the brain and disrupts voltage-gated Na+ (Nav) channels, particularly in fast-spiking parvalbumin (PV) interneurons. These interneurons are essential for maintaining excitatory-inhibitory (E/I) balance, regulating hippocampal-cortical synchronization, and supporting social and spatial memory; all processes disrupted in NDDs. Our breakthrough studies show that early-life DM exposure disrupts PV interneuron firing, alters E/I balance, impairs hippocampal plasticity, and disrupts social memory in mice. These changes are accompanied by reduced PV expression and degradation of perineural nets. Remarkably, acute chemogenetic activation of hippocampal PV interneurons using DREADDs restores both circuit and behavioral deficits, providing a mechanistic link between PV dysfunction and NDD-like phenotypes. We hypothesize that early-life DM exposure impairs PV interneuron structure and circuit integration, leading to memory deficits and brain hyper-connectivity that can be reversed through acute and chronic PV interneuron activation. Using a validated mouse model, we will combine imaging and mass spectrometry (Aim 1), patch-clamp electrophysiology (Aim 2), and behavioral and in vivo electrophysiology assays (Aim 3). This work is expected to define causal links between neurotoxic exposure and NDDs, while identifying PV interneurons as a transdiagnostic target for intervention in exposure-related ASD and ADHD.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2026 ( Subtotal = $722,883 )
2026	2026	UNIVERSITY OF TEXAS MEDICAL BRANCH AT GALVESTON	301 UNIVERSITY BLVD	GALVESTON	TX	77555	GALVESTON	USA	Environmental Health	000	1	9/16/2026	NEW	$722,883
														Subtotal = $722,883

Grand Total All Awards = $722,883

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Hippocampal Vulnerability to Environmental Pesticide Exposure

Award Number: R01ES038738

ORGANIZATION: NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)

PERIOD OF PERFORMANCE START DATE: 09/16/2026

PERIOD OF PERFORMANCE END DATE: 06/30/2031

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