Work

Decreased Oxytocin Mediates PVN–CA2 and PVN–PrL in Sleep Deprivation-Induced Social Memory Deficits

Year: 2025

Type: article

Abstract: While sleep disorders are a known correlate of social memory deficits, the underlying neurocircuitry and molecular mechanisms remain poorly understood. Using an oxytocin (OXT)-specific sensor imaging approach, we discovered that chronic sleep deprivation (SD) reduced OXT neuropeptide release in the hippocampal CA2 and prelimbic cortex (PrL), thereby disrupting social memory encoding and retrieval processes, respectively. Using fiber photometry recordings and in vitro electrophysiology, we identified the activity of the predominantly OXT-expressing neurons in the paraventricular hypothalamic nucleus (PVN OXT ) were reduced following SD. Specific optogenetic activation of the PVN OXT –CA2 pathway during encoding phase or PVN OXT –PrL pathway during retrieval transiently restored SD-induced social memory deficits. Conversely, optogenetic high-frequency activation of PVN OXT neurons enhanced the function of both PVN OXT –CA2 and PVN OXT –PrL pathways, promoting increased OXT release and providing sustained protection against SD-induced social memory deficits. These findings offer causal evidence that the PVN OXT –CA2 and PVN OXT –PrL pathways exert distinct modulatory roles in sleep-related social memory deficits and thereby nominate these pathways as precise targets for neuromodulation in sleep-related cognitive disorders.

Source: Research

DOI: 10.34133/research.1076