EXPRESSION OF FETAL-ALZ-50-REACTIVE-CLONE-1 (FAC1) IN DENTATE GYRUS FOLLOWING ENTORHINAL CORTEX LESION

The Fetal ALZ-50 Reactive Clone 1 (FAC1) gene is expressed at high lev els during brain development and is re-expressed in some neurodegenera tive diseases. It is hypothesized that FAC1 functions during neuronal differentiation and may play an active role in neuritic re-organizatio n following brain injury. We have previously employed the entorhinal c ortex lesion model to examine reactive synaptogenesis and plasticity i n the hippocampal dentate molecular layer following denervating lesion . We now report re-expression of FAC1 in the molecular layer (ML) of t he dentate gyrus following entorhinal cortex (ERC) lesion. Denervated hippocampi (2,6,15, and 30 days post ERC lesion) were stained with ant i-FAC1 antibody and processed for both light and electron microscopy. FAC1 was rapidly re-expressed (by 2 days) following ERC lesion, parall eling our previous observations with embryonic neural cell adhesion mo lecule (eN-CAM). Like eN-CAM, FAC1 expression was restricted to the de nervated outer ML (OML) at 2 days post lesion. Analysis of later time points revealed an elimination of FAC1 immunostaining at the inner ML (IML)/(OML) interface as IML sprouts into the denervated zone. Image a nalysis confirmed the diminution of FAC1 staining in the OML as the IM L sprouted into the denervated zone and revealed that FAC1 expression paralleled the temporal and spatial expression of eN-CAM following ERC lesion. Ultrastructural analysis of FAC1 staining at 6 and 30 days po st lesion revealed immunoreactive profiles with the morphological char acteristics of dendrites and cytoplasmic staining of granule cell peri karya. Dendritic staining was localized to the denervated OML and was not associated with any other neuropil profiles within this zone; IML staining was rare and restricted to large apical dendrites proximal to granule cell perikarya. These findings suggest that re-expression of FAC1 in the denervated OML is a rapid response to brain injury and may be important in synaptic plasticity and sprouting. (C) 1997 Wiley-Lis s, Inc.