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Comment
. 2023 Sep 12;56(9):1983-1985.
doi: 10.1016/j.immuni.2023.08.013.

Astrocytes on steroids binge on synapses to cope with stress

Michael A Wheeler  1 , Francisco J Quintana  2
Affiliations
Comment

Astrocytes on steroids binge on synapses to cope with stress

Michael A Wheeler et al. Immunity. .

Abstract

Many mechanisms by which stress mediates its effects within the central nervous system still remain unknown. Byun, Kim, Kim et al. find that early-life stress triggers corticosterone release to drive astrocyte-dependent synapse elimination and altered behavior. Thus, this work defines a steroid-sensitive astrocyte transcriptional circuit controlling behavior, highlighting how the study of CNS immunoregulation may shed light on behavior.

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Conflict of interest statement

Declaration of interests The authors declare no competing interests.

Figures

Figure 1.
Figure 1.. Glucocorticoids released during stress drive cortical synapse elimination via astrocyte MERTK
In response to early-life stress, increased production of the endogenous glucocorticoid, corticosterone, triggers glucocorticoid receptor (GR)-driven expression of the phagocytic receptor Mertk in astrocytes. Elevated MERTK expression boosts astrocyte phagocytosis of excitatory synapses. In adulthood, mice previously subjected to early-life stress show decreased synaptic density, altered neural activity patterns, and increased helplessness behavior. OFC, orbitofrontal cortex; S1, primary somatosensory cortex.
See this image and copyright information in PMC

Comment on

References

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