Preservation of binocularity after monocular deprivation in the striate cortex of kittens treated with 6‐Hydroxydopamine

The results of single unit recordings from Area 17 of monocularly deprived kittens were compared with similar ones from littermates who had been monocularly lid‐sutured for the same period of time, but who had in addition been given intraventricular injections of 6‐hydroxydopamine (6‐OHDA) to deplete brain catecholamines. The visual cortices of all catecholamine‐depleted kittens showed high proportions of binocular neurons, in contrast to the control group, a majority of whose visual cortical neurons were driven exclusively by the non‐deprived eye. Preservation of binocularity in 6‐OHDA‐treated kittens was dose‐related. Even after a 1 to 2‐week period of lidsuture which reduced binocularity to 20% in controls, normal proportions of binocular neurons (>75%) were preserved if the cumulative dose had been 10 mg 6‐OHDA or more. The density of single neurons sampled from electrode tracks through the cortex of drug‐treated kittens was high and did not differ significantly from controls. Neurons were isolated every 100 μm on the average. There was some indication that the drug's effect in preventing an ocular dominance shift disappears by six weeks following cessation of 6‐OHDA treatment. This reversal of the physiological effects in cortex is preceded by recovery from the behavioral manifestations of 6‐OHDA treatments. Binocularity was only slightly increased in a kitten who received large doses of 6‐OHDA after a period of monocular deprivation. This observation, together with control recordings from normal kittens and adults treated with 6‐OHDA, indicates that the direct effects of 6‐OHDA on cortical neurons' response properties play a minor role in comparison to its effects in reducing the sensitivity of the cortex to monocular deprivation. The overwhelming majority of cortical neurons in 6‐OHDA‐treated kittens remained normal in receptive field properties after a period of monocular deprivation. These data support the hypothesis that catecholamines are required for the maintenance of visual cortical plasticity during the critical period.