Difference and relationship between plastic synapse of sensitive period and that of after effect in the visual cortex.

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Since the pioneering work by Wiesel and Hubel in 1963, involvements of (i) the activity-dependent mechanism and (ii) the neurochemical basis, have been suggested in the regulation of the ocular doinance plasticity observed during the sensitive period. We have proposed that the central noradrenergic system plays a crucial role in the regulation of the ocular dominance plasticity as a major neurochemical basis. Recent electron microscopic studies showed that astrocytes in kitten visual cortex express beta-adrenergic receptors. Thus, we consider a possibility that the action of noradrenaline (NA) is partially mediated by the astrocytic function and immature astrocytes may integrate the activity-dependent mechanism and the neurochemical basis. We have shown that a gliotoxin suppressed the ocular dominance plasticity. This glial involvement may be unique for the sensitive period plasticity not for the aftereffect. We studied after effects using adequate drifting since wave grating.Fifty percent of cells in area 17 examined showed aftereffect. The lower frequency of aftereffect seems to depend on the anesthesia and paralysis. It has priviously been demonstrated that ocular dominance plasticity is freezed under anesthetized and paralyzed conditions. Although, these finding may be correlated each other, we could not detect the increase of frequency of cells showing aftereffect by the NA indusion. Experiments with the monocularly deprived kitten showed that the conditioning of the deprived eye never induced aftereffect of the normal eye, suggested that synapses of aftereffect are affected by visual environment during the sensitive period.