The nature of the sustained norepinephrine-induced depolarization in brown fat cells was examined by patch-clamp techniques. Norepinephrine (NE) stimulation led to a whole cell current response consisting of two phases: a first inward current, lasting for only 1 min, and a sustained inward current, lasting as long as the adrenergic stimulation was maintained. The nature of the sustained current was here investigated. It could be induced by the ₁-agonist cirazoline but not by the ₃-agonist CGP-12177A. Reduction of extracellular Cl concentration had no effect, but omission of extracellular Ca²⁺ or Na⁺ totally eliminated it. When unstimulated cells were studied in the cell-attached mode, some activity of 30 pS nonselective cation channels was observed. NE perfusion led to a 10-fold increase in their open probability (from 0.002 to 0.017), which persisted as long as the perfusion was maintained. The activation was much stronger with the ₁-agonist phenylephrine than with the ₃-agonist CGP-12177A, and with the Ca²⁺ ionophore A-23187 than with the adenylyl cyclase activator forskolin. We conclude that the sustained inward current was due to activation of 30 pS nonselective cation channels via ₁-adrenergic receptors and that the effect may be mediated via an increase in intracellular free Ca²⁺ concentration.