Local perfusion of noradrenaline maintains visual cortical plasticity

Abstract

WE have formed a hypothesis which links two important, but so far separate, research areas, the monoaminergic system discovered by the Swedish group^1,2 and the phenomenon of critical period plasticity in the visual cortex discovered by Wiesel and Hubel^3,4. We propose⁵ that the widespread system of monoaminergic fibres plays a part in regulating plasticity and that, more specifically, catecholamines are responsible for maintaining the high level of plasticity which is observed in the visual cortex during the critical period⁴. In an initial test of this hypothesis, we developed a dose and timing regimen of 6-hydroxydopamine (6-OHDA) to produce significant depletion of catecholamines bilaterally in the visual cortex of developing kittens⁵. The hypothesis was confirmed to the extent that kittens treated with 6-OHDA do not have the usual cortical plasticity, as measured by a change in the ocular dominance of binocular neurones following monocular occlusion⁵. While all the results we have obtained so far with 6-OHDA are consistent with the view that catecholamines regulate cortical plasticity, other interpretations are possible because of the widespread nature of the changes accompanied by intraventricular 6-OHDA. We now present further evidence in support of the hypothesis from experiments involving microperfusion of catecholamine in localised areas of the visual cortex of animals which would not be expected to show plasticity. These experiments indicate a specific role of noradrenaline (NA) within the cortex because plastic changes are found only in the region of cortex perfused by NA while nearby cortical regions in the same kitten are unaffected.