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Reorganization of the Rat Fascia Dentata after a Unilateral Entorhinal Cortex Lesion: Role of the Extracellular Matrix
Author(s) -
DELLER THOMAS,
HAAS CAROLA A.,
FROTSCHER MICHAEL
Publication year - 2000
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2000.tb06728.x
Subject(s) - fascia dentata , entorhinal cortex , sprouting , extracellular matrix , chondroitin sulfate proteoglycan , neuroscience , microbiology and biotechnology , proteoglycan , axon , chemistry , hippocampus , anatomy , biology , dentate gyrus , botany
A bstract : Entorhinal cortex lesion (ECL) partially denervates the fascia dentata of the hippocampus. This is said to induce the sprouting of intact fibers from neighboring layers that invade the zone of the degenerating axons. However, recent studies using anterograde tracing failed to demonstrate sprouting across laminar boundaries. Sprouting does occur, but it mainly involves unlesioned fiber systems terminating within the layer of fiber degeneration. It is now of interest to identify the cues that could underlie this layer‐specific sprouting response. Since extracellular matrix (ECM) molecules delineate boundaries of axonal growth during development, it was tested whether these molecules play a similar role during the sprouting process following ECL. After ECL, reactive astrocytes rapidly synthesize and secrete growth‐inhibiting ECM molecules, such as tenascin‐C and the chondroitin sulfate proteoglycan neurocan, into the ECM of the outer molecular layer. These molecules form a sharp border against the nondenervated inner molecular layer. This pattern of ECM molecule expression may contribute to the layer‐specific sprouting response of surviving afferents after ECL: axons trying to grow into the denervated outer molecular layer, for example, from the inner molecular layer, would be deflected by a growth‐inhibiting ECM barrier.