Molecular mechanisms underlying the metamorphosis of larvae, e.g., ligand and receptor interaction, have to be determined and roles for the nervous system in marine invertebrates are not well understood. We report here that treatment of swimming larvae of the ascidian Ciona savignyi with noradrenaline or adrenaline promoted morphological changes in early metamorphosis, e.g., tail resorption. Antagonists of the β-adrenergic receptor, propranolol, and the β 1-adrenergic receptor, metoprolol, inhibited the noradrenaline-induced tail resorption, while an antagonist of the α-adrenergic receptor, phentolamine, and of the β 2- adrenergic receptor, butoxamine, had no inhibitory effects. In addition, a selective agonist of the β-adrenergic receptor, isoproterenol, the concentration of which was lower than the effective concentration of the neurotransmitters, facilitated tail resorption. Immunohistochemical studies, using an anti-dopamine-hydroxylase antibody, showed that neurotransmitters such as noradrenaline and adrenaline localized around the brain vesicle of the larvae during metamorphosis. The β 1-adrenergic receptor stained with antibodies was localized on the nervous system. Temporal expression of the β 1-adrenergic receptor was intense in the nervous system in the larvae competent for metamorphosis. We propose that interactions between noradrenaline or adrenaline and the β 1-adrenergic receptor in the nervous system mediate the process of metamorphosis of Ciona larvae.