Planar cell polarity proteins mediate ketamine-induced restoration of glutamatergic synapses in prefrontal cortical neurons in a mouse model for chronic stress

Andiara E. Freitas, Bo Feng, Timothy Woo, Shae Galli, Clayton Baker, Yue Ban, Jonathan Truong, Anna Beyeler and Yimin Zou ()
Additional contact information
Andiara E. Freitas: San Diego
Bo Feng: San Diego
Timothy Woo: San Diego
Shae Galli: San Diego
Clayton Baker: San Diego
Yue Ban: San Diego
Jonathan Truong: San Diego
Anna Beyeler: Rue Leo Saignat
Yimin Zou: San Diego

Nature Communications, 2024, vol. 15, issue 1, 1-12

Abstract: Abstract Single administration of low-dose ketamine has both acute and sustained anti-depressant effects. Sustained effect is associated with restoration of glutamatergic synapses in medial prefrontal cortic (mFPC) neurons. Ketamine induced profound changes in a number of molecular pathways in a mouse model for chronic stress. Cell-cell communication analyses predicted that planar-cell-polarity (PCP) signaling was decreased after chronic administration of corticosterone but increased following ketamine administration in most of the excitatory neurons. Similar decrease of PCP signaling in excitatory neurons was predicted in dorsolateral prefrontal cortical (dl-PFC) neurons of patients with major depressive disorder (MDD). We showed that the basolateral amygdala (BLA)-projecting infralimbic prefrontal cortex (IL PFC) neurons regulate immobility time in the tail suspension test and food consumption. Conditionally knocking out Celsr2 and Celsr3 or Prickle2 in the BLA-projecting IL PFC neurons abolished ketamine-induced synapse restoration and behavioral remission. Therefore, PCP proteins in IL PFC-BLA neurons mediate synapse restoration induced by of low-dose ketamine.

Date: 2024
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DOI: 10.1038/s41467-024-48257-6

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