Adolescent stress remodels synapses in the sensory thalamus and impairs tactile discrimination in mice

TL;DR

Adolescent stress in mice changes brain circuits for touch, leading to trouble sensing fine textures, and these changes can be partly reversed by social interaction.

Contribution

The study reveals that adolescent stress, not adulthood stress, alters thalamic circuits via glucocorticoid receptors, impairing tactile discrimination.

Findings

Adolescent social isolation increases afferent connections but weakens individual synaptic strength in the sensory thalamus.

Mice with adolescent isolation show impaired tactile discrimination due to altered thalamic circuitry.

Social cohabitation can partially reverse the synaptic effects of adolescent isolation.

Abstract

Adolescent stress can lead to persistent behavioral issues and brain dysfunction, often linked to sensory perception abnormalities. The biological basis for these sensory changes is not well understood. Here, we demonstrate that social isolation during adolescence, but not adulthood, remodels the structure and function of brain circuits that process touch in mice. Specifically, isolation increases the number of afferents to each neuron while weakening individual connections, and these changes depend on the activation of glucocorticoid receptors in thalamic neurons. Mice exposed to adolescent isolation also show reduced ability to distinguish fine tactile differences, suggesting a functional impact of the altered thalamic circuitry. Cohabitation with another mouse can partially reverse the synaptic effects of adolescent isolation. Our findings identify the sensory thalamus as a vulnerable site for adolescent stress and show how social experiences during this period can remodel sensory circuits, providing new directions for preventing or treating stress-related sensory problems.

Adolescent social isolation remodels somatosensory thalamic circuits via glucocorticoid receptors, impairing tactile discrimination. These findings reveal a stress-sensitive mechanism linking social experience to sensory dysfunction.

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