Spontaneous helping behaviors such as allogrooming are vital for survival in social species, yet their underlying neural mechanisms remain largely unknown. Although oxytocin (OXT) is known to modulate allogrooming, the precise neural circuits, molecular pathways, and sensory drivers remain unclear. Here, using a social emergency paradigm in mice, we show that observer mice selectively allogroom distressed, anesthetized conspecifics, a behavior that is guided by main olfactory system cues and mitigates the demonstrator anxiety. We identify an oxytocinergic circuit from the paraventricular hypothalamus to the medial olfactory tubercle (PVNOXT-mOT) that is necessary and sufficient for this helping behavior. In vivo fiber photometry reveals that PVNOXT-mOT activity and OXT release are temporally locked to allogrooming initiation. This behavioral effect requires oxytocin receptor (OXTR) signaling specifically on mOT dopamine D1 receptor-expressing neurons, where OXTRs suppress neuronal excitability via G protein-gated inwardly rectifying K+ (GIRK) channels. Disruption of this inhibitory mechanism induces neuronal hyperexcitability and impairs allogrooming, a deficit rescued by restoring GIRK function. These findings define a PVNOXT-mOT circuit for prosocial helping, revealing an oxytocinergic pathway with potential therapeutic relevance for neuropsychiatric disorders characterized by social deficits.
Depression subtype classification from social media posts: few-shot prompting vs. fine-tuning of large language models
BackgroundSocial media provides timely proxy signals of mental health, but reliable tweet-level classification of depression subtypes remains challenging due to short, noisy text, overlapping symptomatology,