Crossed pathways from the entorhinal area to the fascia dentata. II. Provokable in rats

Abstract

In the rat the perforant pathways from the entorhinal area normally innervate the fascia dentata only ipsilaterally. However, unilateral ablation of the entorhinal area (deentorhination) induces the formation of an anomalous crossed projection from the intact contralateral entorhinal area to the septal portion of the deafferented fascia dentata. After deentorhination of rats aged from 1–30 days the organization of this projection was analyzed (a) by producing secondary lesions in the intact entorhinal area or perforant paths and observing the resulting anterograde degeneration with Fink-Heimer silver impregnation techniques, and (b) by staining with Timm's sulfide silver method which makes the terminal fields of afferent systems stand out in different tones or colors. Both methods showed the crossed entorhino-dentate projection to consist of two separable components. They were named the crossed medial perforant path and the crossed lateral perforant path, corresponding to their similarity in origin, dendritic localization of termination and Timm stainability to the ordinary, uncrossed medial and lateral perforant pathways (MPP and LPP) which arise in the medial and the lateral parts of the entorhinal cortex, respectively. Similarly induced crossed projections were demonstrated to the subcallosal continuation of fascia dentata, the fasciola cinerea. The heaviest terminal field of the crossed entorhino-dentate projection which was found in the most rostral and medial parts of the deafferented fascia dentata correlated with a lack of expected aberrant extension into the MPP and LPP terminal zones of commissural and ipsilateral hippocampodentate fibers. In Fink-Heimer preparations there was little variation in the distribution of the aberrant crossed systems over the range of ages studied although the chronic operations performed earliest postnatally (5 days) tended to produce the heaviest representation. This latter observation appeared consistent with changes in the Timm staining pattern of the deafferented fascia dentata, since with an increase in age at the primary lesion from 5 to 14 days there was an increase in the spread into the fascia dentata of Timm stainable axon terminals from CA3, interpreted as a sign of fewer crossed entorhinal afferents succeeding in a presumable competition with the CA3-derived system for available terminal space. The CA3-derived terminals distributed in an intermediate band in the dentate molecular layer beneath the zones occupied by the crossed entorhinal projections. The appearance of a similarly placed, but less intense intermediate band of Timm staining on the side contralateral to the chronic lesion was observed. This is tentatively interpreted as an indication that a normal crossed entorhinodentate projection does exist, its removal having caused a spread of Timm stainable terminals from the adjacent CA3. Both careful light microscopic analysis of the degeneration picture which followed acute entorhinal lesions of control animals as well as preliminary electron microscopic studies further indicated the existence of a sparse crossed entorhino-dentate projection in normal rats. In the rabbit the existence of a normal crossed entorhino-dentate projection has been demonstrated by the authors in an accompanying study. The differences in the morphology of the most septal parts of the fascia dentata and fasciola cinerea of the rat and the rabbit provided an excellent opportunity for evaluation of the role of spatial and temporal factors involved in the regulation of the growth of axons of entorhinal origin.