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Prenatal methadone exposure selectively alters protein expression in primary motor cortex: Implications for synaptic

David L Haggerty1, Gregory G Grecco1,2, Jui-Yen Huang3,4

  • 1Department of Pharmacology and Toxicology, Indiana University School of Medicine, Indianapolis, IN, United States.

Frontiers in Pharmacology
|February 23, 2023
PubMed
Summary

Prenatal methadone exposure (PME) in mice alters offspring brain development, particularly in the primary motor cortex (M1). PME uniquely impacts M1 synaptic function and anatomy, suggesting a target for future interventions.

Keywords:
glutamatergic synapsemethadonemotor cortexneurodevelopmentprenatal opiate exposureproteomics & bioinformatics

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Area of Science:

  • Neuroscience
  • Developmental Biology
  • Pharmacology

Background:

  • Opioid use disorder (OUD) in pregnant women is rising, increasing risks for offspring neurodevelopment.
  • Prenatal opioid exposure causes sensorimotor deficits and hyperactivity in offspring.
  • Mechanisms linking prenatal opioid exposure to brain changes are not fully understood.

Purpose of the Study:

  • To investigate the molecular and anatomical changes in the developing brain of offspring exposed to methadone during gestation.
  • To identify specific brain regions and synaptic pathways affected by prenatal methadone exposure (PME).

Main Methods:

  • Used a mouse model of prenatal methadone exposure (PME).
  • Conducted unbiased multi-omic analysis (proteomics and phosphoproteomics) on sensorimotor brain regions.
  • Performed gene ontology enrichment and immunohistochemical analysis.

Main Results:

  • PME induced widespread changes in protein and phosphopeptide abundance across brain regions.
  • The primary motor cortex (M1) was uniquely affected, showing altered glutamatergic and GABAergic synapse densities.
  • Conserved phosphopeptide changes related to synaptic activity were observed brain-wide, but protein changes were specific to M1.

Conclusions:

  • Prenatal methadone exposure causes lasting synaptic alterations in the offspring's brain, with M1 being a key region.
  • Protein and anatomical changes in M1 are critical for understanding PME's neurodevelopmental effects.
  • Findings provide a basis for developing interventions against adverse PME outcomes.