Monoaminergic afferents to cortex modulate structural plasticity in the barrelfield of the mouse

Abstract

Electrolytic lesions of the follicles of a set of mystacial vibrissae, and their innervation, of the mouse placed during the early postnatal period result in a modification in appearance of the corresponding and of adjacent barrels in the somatosensory cortex of the adult animal. These changes can be evoked during the first 6 days of postnatal life — the so-called critical period. The pattern of these modifications varies with the age of the animal at which the lesion was placed. In order to evaluate the contribution of the monoaminergic cortical input to this type of plasticity, the noradrenergic and/or serotonergic afferents to the cerebral cortex of newborn mice were destroyed by systemic administration of various selective neurotoxic drugs (6-hydroxydopamine, 5,7-dihydroxytryptamine, N-(2-chloroethyl)- N-ethyl-2-bromobenzylamine). The animals were then subjected, on postnatal day 3 (P3; PO = day of birth), to a lesion of the follicles of the large, caudal mystacial vibrissae of row C. Control animals were injected with vehicle solution only but had the same follicles lesioned. Compared with animals with intact monoaminergic afferents, those treated with neurotoxins showed a different changed barrel pattern, i.e. one that corresponded to a pattern normally obtained after a lesion placed at an earlier stage of development, i.e. at P2 or P1. Thus, monoaminergic depletion of the cortex results in a retardation of the maturation of the parietal cortex as defined by its plastic response to peripheral nerve injury. Interestingly, a peripheral lesion at P4 yields barrel patterns in monoamine deprived mice similar to those in controls, as if monoamines at that stage play no longer a role in this form of brain plasticity.