Crosstalk between maternal perinatal obesity and offspring dopaminergic circuitry
Yuki Yasumoto, Tamas L. Horvath
Yuki Yasumoto, Tamas L. Horvath
Published June 8, 2020
Citation Information: J Clin Invest. 2020;130(7):3416-3418. https://doi.org/10.1172/JCI138123.
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Commentary

Crosstalk between maternal perinatal obesity and offspring dopaminergic circuitry

Abstract

The mechanism by which maternal obesity influences fetal brain development and behavior is not well understood. In this issue of the JCI, Lippert et al. showed that feeding maternal mice a high-fat diet (HFD) during lactation attenuated the activity of dopamine (DA) midbrain neurons and altered the DA-related behavioral phenotype seen in the offspring. The authors further suggested that the altered excitatory and inhibitory balance between D1 medium spiny neurons (MSN) and D2 MSN mediates this behavioral phenotype. These mechanisms may provide strategies for preventing the negative effects of maternal obesity on offspring development and adult health.

Authors

Yuki Yasumoto, Tamas L. Horvath

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Figure 1

HFD induces alterations in the midbrain dopaminergic circuitry with behavioral outcome.

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HFD induces alterations in the midbrain dopaminergic circuitry with beha...
(A and B) Lippert et al. (9) showed that feeding maternal mice an HFD during lactation reduced DA midbrain neuronal activity and altered offspring behavior. D1 MSNs showed increased activity, while D2 MSNs displayed decreased neuronal projections in the GP and VP.