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Physiological stimuli operative during, for example, dehydration or lactation, induce neurohypophysial astrocytes (pituicytes) to undergo reversible morphological changes, which in turn may modulate the release of vasopressin and oxytocin. To study the molecular mechanisms of this morphological plasticity, we used primary cultures of rat pituicytes. During stimulation with adenosine, pituicytes become stellate, which is characterized by a round, phase-bright soma and complex arborization, implying major cytoskeletal modifications. Following addition of vasopressin or oxytocin, stellate pituicytes revert to a flat shape. The effects of both hormones are mediated by V1a receptor activation, which also induces biphasic Ca2+i signals in pituicytes. Stellation reversal requires Ca2+-dependent activation of Cdc42, a small GTPase known to impact on the cytoskeleton. V1a receptor activation by vasopressin or oxytocin also stimulates [3H]taurine efflux from cultured pituicytes. As taurine inhibits vasopressin output from neurohypophysial terminals, we postulate a negative-feedback mechanism whereby secreted vasopressin limits its own availability. This stop signal might be reinforced by shape changes elicited by vasopressin in pituicytes. These results support the concept that, during specific physiological states, pituicyte V1a receptor activation modulates the release of neurohypophysial hormones.