ArticleiScience2024
Robust GRK2/3/6-dependent desensitization of oxytocin receptor in neurons.
Article in iScience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- A heteromeric TRP channel that functions as a WNT-activated G protein-coupled receptor.Nature communications · 2026Article
- Context-dependent oxytocin receptor signaling: from molecular architecture to transcript-level receptor engineering.Frontiers in neuroscience · 2026Review
- Oxytocinergic signalling in the respiratory parafacial region increases the activity of chemosensitive neurons and respiratory output.The Journal of physiology · 2025Article
- Input-specific properties of excitatory synapses on oxytocin receptor-expressing neurons in the lateral septum.Journal of neurophysiology · 2024Article
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Authors and funding
7 authors.
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Abstract
Oxytocin plays critical roles in the brain as a neuromodulator, regulating social and other affective behavior. However, the regulatory mechanisms controlling oxytocin receptor (OXTR) signaling in neurons remain unexplored. In this study, we have identified robust and rapid-onset desensitization of OXTR response in multiple regions of the mouse brain. Both cell autonomous spiking response and presynaptic activation undergo similar agonist-induced desensitization. G-protein-coupled receptor kinases (GRK) GRK2, GRK3, and GRK6 are recruited to the activated OXTR in neurons, followed by recruitment of β-arrestin-1 and -2. Neuronal OXTR desensitization was impaired by suppression of GRK2/3/6 kinase activity but remained unaltered with double knockout of β-arrestin-1 and -2. Additionally, we observed robust agonist-induced internalization of neuronal OXTR and its Rab5-dependent recruitment to early endosomes, which was impaired by GRK2/3/6 inhibition. This work defines distinctive aspects of the mechanisms governing OXTR desensitization and internalization in neurons compared to prior studies in heterologous cells.
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