6-OH-DA is an isomer of noradrenalin which is selectively taken up by adrenergic axons. Noradrenalin stores are displaced by 6-OH-DA and at a certain intraneuronal concentration, degeneration of the terminals occurs and results in a chemical sympathectomy. The effects of 6-OH-DA on the rabbit cochlea were studied with fluorescence and electron microscopy after systemic administration of the substance and after local perfusion of the cochlea. Doses of 25 to 200 mg/kg were used. After intravenous injection there was an initial accumulation of 6-OH-DA in noradrenalin storage vesicles. A dose of 50 mg/kg 6-OH-DA initiated marked signs of degeneration in adrenergic nerve terminals but did not cause breakdown of their cell membranes. Higher doses did not seem to increase the damage. Local perfusion with 6-OH-DA gave rise to extensive degeneration of adrenergic nerve terminals and after 7 days all terminals had disappeared. These findings indicate the presence of a blood-perilymph barrier to 6-OH-DA. Some degeneration was also evident in cholinergic axons of the inner spiral bundle and of the tunnel spiral bundle.