EFFECT OF COLLATERAL SPROUTING ON THE DENSITY OF INNERVATION OF NORMAL TARGET SITES - IMPLICATIONS FOR THEORIES ON THE REGULATION OF THE SIZE OF DEVELOPING SYNAPTIC DOMAINS

The 'commissural' innervation of the denate gyrus molecular layer has been analyzed in normal adult rats and in those in which the ipsilateral entorhinal cortex had been removed by aspiration at 14 days post-natal. This ablation severely deafferents the distal two-thirds of the molecular layer and induces 'sprouting' by the commissural afferents which are normally restricted to the more proximal dendritic zone. It was the objective of the present study to employ quantitative electron microscopy to determine (1) the extent of synaptic recovery in the deafferented field; (2) the magnitude of the contribution by the commissural fibers to the reinnervation of the deafferented field; and (3) if sprouting by the commissural projections causes a reduction in the density of the terminal field they generate in their normal target region. The synaptic density of the neonatally deafferented middle molecular layer was found to have returned to near control levels by adulthood. Degeneration studies performed in the adult revealed that commissural endings were located in equivalent numbers in the inner and middle molecular layers of rats in which the entorhinal cortex had been removed at 14 days post-natal; in normal rats (i.e. no neonatal surgery) the commissural terminals were found only in the inner molecular layer. Furthermore, and most importantly, the density of commissural terminals in the inner molecular layer was virtually identical in the 'sprouted' and control rats. Thus the tremendous areal expansion of the commissural terminal field which occurs after early deafferentation of the distal parts of the granule cell dendrites was not accompanied by any loss of input to the normal target of this afferent. Therefore, sprouting in this system represents an exaggeration of normal growth rather than a redistribution of a fixed population of endings. The relevance of these findings to theories concerned with the regulation of axonal growth and terminal proliferation during development is discussed. © 1979.