Oxytocin (OXT) is a hypothalamus-derived neuropeptide majorly secreted via the posterior pituitary. In OXT neurons, dendritic and axonal synapses store and release OXT during social and reproductive behavior. Reduced hypothalamic OXT content and genetic polymorphisms in oxytocin receptor are observed in autism-like mice models and socially-impaired children respectively. These observations led to the controversial OXT-deficit hypothesis of autism spectrum disorders. Thus, investigating the molecular mechanisms that regulate synaptic OXT content and release are essential to understand autism spectrum disorders.
At a molecular level, astrocyte-like cells, pituicytes that are closely-associated with the neurohypophyseal axonal terminals can secrete factors that affect OXT content or release. However, the identity and the role of pituicyte-derived secreted factors that can regulate synaptic OXT are largely unknown. Finally, situated outside the blood-brain barrier (BBB), pituicytes are directly exposed to the blood-borne molecules and are highly responsive to physiological challenges to promote synaptic plasticity. But the identity and the role of the pituicyte-derived cues that regulate OXT axonal terminals and OXT neuropeptide content upon challenges are largely unknown.
The research aim of the group is to identify challenge-induced pituicyte-derived secreted factors that regulate neurohypophyseal synaptic OXT content.
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