Affiliations: Department of Clinical Neuroanatomy, J. W Goethe
University, Theodor-Stern-Kai 7, D-60590 Frankfurt/Main, Germany | lnstitute of Anatomy, University of Freiburg, P O. Box
111, D-79001 Freiburg, Germany
Note: [] Corresponding author: Thomas Deller, M.D., Department of
Clinical Neuroanatorny, J. W. Goethe University, Theodor-Stem-Kai 7, D-60590
Frankfurt/Main, Germany. Tel.: +49 69 6301 6361; Fax: +49 69 6301 6425; E-mail:
T.Deller@em.uni-frankfurt.de.
Abstract: Entorhinal cortex lesion partially denervates the rat fascia
dentata. This is said to induce sprouting of intact fibers from neighboring
layers that invade the zone of the degenerating axons. However, recent in vivo
and in vitro studies failed to demonstrate sprouting across laminar boundaries.
Sprouting does occur, but it mainly involves unlesioned fiber systems
terminating within the layer of fiber degeneration. These findings point to
laminar cues that promote sprouting of fibers within the denervated zone while
repelling other, adjacent fiber systems that try to grow into the denervated
zone. A group of molecules that are likely to guide the sprouting process and
the formation of borders are extracellular matrix molecules synthesized by
reactive astrocytes. These molecules provide boundaries for growing axons
during development. Some extracellular matrix molecules (tenascin-C, DSD- 1
-proteoglycan, neurocan, and brevican) were upregulated within the denervated
outer molecular layer after lesion of the entorhinal cortex, suggesting a
similar role after lesion. These extracellular matrix components forin a sharp
molecular border towards the adjacent nondenervated inner molecular layer, and
their pattern of distribution correlates precisely with the laminar termination
pattern of the sprouting fiber populations. Thus, extracellular matrix
molecules could delineate boundaries of axonal growth after entorhinal cortex
lesion and could thus contribute to the molecular processes underlying the
postlesional re-patterning of the fascia dentata.
