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Abstract
Chemogenetic activation of the infralimbic cortex induces rapid antidepressant-like effects in a mouse model of stress-induced depression.
- Activation of the infralimbic cortex enhances structural plasticity in the hippocampus.
- Restoration of long-term potentiation deficits occurs following infralimbic cortex stimulation.
- The thalamic nucleus reuniens is identified as a necessary mediator for these effects.
- Inhibition of the nucleus reuniens or its pathways blocks both the antidepressant response and neuroplastic effects associated with infralimbic cortex stimulation and ketamine treatment.
- The infralimbic cortex to nucleus reuniens to ventral hippocampus circuit is crucial for linking circuit activity, hippocampal plasticity, and depressive-like behaviors.
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