PubMed1985
A quantitative re-examination was made of the influence of noradrenergic depletion on the epigenesis of kitten visual cortex. Two methods were used to deplete noradrenaline at the cortical level: stereotaxically controlled injection of 6-hydroxydopamine (6-OHDA) in the coeruleus complex, from which the noradrenergic input to visual cortex arises; intraventricular injection of 6-OHDA. The latter chemical lesion also depleted dopamine levels in the brain. Lesion of the noradrenergic or catecholaminergic systems was performed neonatally or at an age of 3-4 weeks in kittens submitted to five different rearing procedures: normal rearing, dark rearing, monocular rearing, monocular exposure following dark rearing and monocular deprivation following normal rearing. Forty-two kittens between 3 and 12 weeks of age were used for this biochemical and electrophysiological study. Noradrenaline and dopamine levels were measured by a radioenzymatic method in the primary visual cortex of twenty-six kittens. A total of 1263 cells were recorded in area 17 of twenty-six kittens. Combined biochemical and electrophysiological data were obtained in ten 6-OHDA-lesioned kittens. Whatever the mode of chemical lesion used, cortical noradrenergic depletion failed to block either maturation or vision-dependent processes which are known to affect orientation selectivity and/or ocular dominance during the critical period. However, in some cases, the amplitude of the epigenetic functional modifications was slightly reduced in 6-OHDA-treated kittens. The cortical effects of monocular deprivation starting from the age of 5 weeks were studied quantitatively both in lesioned and intact kittens. Disappearance of noradrenaline in area 17 did not prevent the loss of binocularity in cortical cells. However, even when monocular occlusion had been maintained for 2 or 3 weeks in 6-OHDA-treated kittens, ocular dominance shifts were limited to a stage equivalent to that observed in the intact kitten after 5-8 days of monocular occlusion. The amplitude of this partial protective effect was found to be unrelated either to the delay following the chemical lesion, or to the level of noradrenaline remaining in lesioned kitten cortex. Although a putative gating role of noradrenaline cannot be excluded in the development of the intact animal, this report shows that its presence is not required for functional plasticity to occur in kitten area 17.