Dissociation-related behaviors in mice emerge from the inhibition of retrosplenial cortex parvalbumin interneurons.
Cell reports January 28, 2025 Yue Hu, Yifan Feng, Huoqing Luo et al. 6 citations
In mice, doses of ketamine that cause dissociation inhibit parvalbumin interneurons (PV-INs) in the retrosplenial cortex (RSC), increasing delta oscillations (1-3 Hz) and delta-gamma phase-amplitude coupling (δ-γ PAC) and producing dissociation-like behaviors. Directly inhibiting these neurons without ketamine also triggers delta oscillations, δ-γ PAC, and some dissociation-like behaviors. Activating RSC PV-INs or knocking down the NMDA receptor subunit NR1 and the HCN1 channel in these neurons reduces ketamine-induced delta oscillations, δ-γ PAC, and certain dissociation-like behaviors. The findings identify NR1 and HCN1 as ketamine targets in PV-INs that may cooperatively affect dissociation, suggesting potential therapeutic targets for dissociative symptoms.