Expression of the neural adhesion molecule L1 in the deafferented dentate gyrus

Standard

Expression of the neural adhesion molecule L1 in the deafferented dentate gyrus. / Jucker, M; D'Amato, F; Mondadori, C; Mohajeri, H; Magyar, J; Bartsch, U; Schachner, M.

in: NEUROSCIENCE, Jahrgang 75, Nr. 3, 12.1996, S. 703-15.

Publikationen: SCORING: Beitrag in Fachzeitschrift/ZeitungSCORING: ZeitschriftenaufsatzForschungBegutachtung

Harvard

Jucker, M, D'Amato, F, Mondadori, C, Mohajeri, H, Magyar, J, Bartsch, U & Schachner, M 1996, 'Expression of the neural adhesion molecule L1 in the deafferented dentate gyrus', NEUROSCIENCE, Jg. 75, Nr. 3, S. 703-15.

APA

Jucker, M., D'Amato, F., Mondadori, C., Mohajeri, H., Magyar, J., Bartsch, U., & Schachner, M. (1996). Expression of the neural adhesion molecule L1 in the deafferented dentate gyrus. NEUROSCIENCE, 75(3), 703-15.

Vancouver

Jucker M, D'Amato F, Mondadori C, Mohajeri H, Magyar J, Bartsch U et al. Expression of the neural adhesion molecule L1 in the deafferented dentate gyrus. NEUROSCIENCE. 1996 Dez;75(3):703-15.

Bibtex

@article{bc534b60ba78401daae9165dc0567607,
title = "Expression of the neural adhesion molecule L1 in the deafferented dentate gyrus",
abstract = "Expression of the neural adhesion molecule L1 and its potential involvement in axonal sprouting were examined in the deafferented rat dentate gyrus. We focused on the dentate gyrus because of its well-defined cytoarchitecture and well-characterized neuronal degeneration and sprouting response following entorhinal cortex lesions. In the molecular layer of the dentate gyrus, a trilaminar staining pattern was observed, with the middle molecular layer exhibiting slightly denser immunolabeling compared to both inner and outer molecular layers. Two to 12 days after a unilateral entorhinal cortex lesion, a progressive loss of L1 immunolabeling was noted in the ipsilateral middle and outer molecular layers, followed by a substantial reappearance of immunostaining 65 days after lesion incidence. The width of the immunostained ipsilateral inner molecular layer revealed a progressive widening and by postlesion day 65 occupied about 50% of the total width of the molecular layer. Immunoelectron microscopy localized L1 to the surface of unmyelinated axons in both normal and deafferented dentate gyrus. In situ hybridization revealed L1 messenger RNA confined to neurons throughout the hippocampal formation, but did not indicate changes in L1 messenger RNA levels in the hippocampus, dentate gyrus, entorhinal cortex or basal forebrain in response to unilateral entorhinal cortex lesions. Changes in L1 immunolabeling in the deafferented dentate gyrus corresponded in a spatial and temporal manner to changes of the synaptic marker synaptophysin and axonal marker phosphorylated tau. Results of the present study are most consistent with the view that L1 is expressed on reinnervating fibers after they make synaptic contacts with other structures. Thus, L1 appears to be involved in the maturation and stabilization of reinnervating fibers and consequently may play an important role in the repair process of the lesioned adult CNS.",
keywords = "Animals, Cell Adhesion Molecules, Neuronal, Cholinergic Fibers, Dentate Gyrus, Hippocampus, Immunohistochemistry, In Situ Hybridization, Male, Rats, Rats, Sprague-Dawley, Journal Article",
author = "M Jucker and F D'Amato and C Mondadori and H Mohajeri and J Magyar and U Bartsch and M Schachner",
year = "1996",
month = dec,
language = "English",
volume = "75",
pages = "703--15",
journal = "NEUROSCIENCE",
issn = "0306-4522",
publisher = "Elsevier Limited",
number = "3",

}

RIS

TY - JOUR

T1 - Expression of the neural adhesion molecule L1 in the deafferented dentate gyrus

AU - Jucker, M

AU - D'Amato, F

AU - Mondadori, C

AU - Mohajeri, H

AU - Magyar, J

AU - Bartsch, U

AU - Schachner, M

PY - 1996/12

Y1 - 1996/12

N2 - Expression of the neural adhesion molecule L1 and its potential involvement in axonal sprouting were examined in the deafferented rat dentate gyrus. We focused on the dentate gyrus because of its well-defined cytoarchitecture and well-characterized neuronal degeneration and sprouting response following entorhinal cortex lesions. In the molecular layer of the dentate gyrus, a trilaminar staining pattern was observed, with the middle molecular layer exhibiting slightly denser immunolabeling compared to both inner and outer molecular layers. Two to 12 days after a unilateral entorhinal cortex lesion, a progressive loss of L1 immunolabeling was noted in the ipsilateral middle and outer molecular layers, followed by a substantial reappearance of immunostaining 65 days after lesion incidence. The width of the immunostained ipsilateral inner molecular layer revealed a progressive widening and by postlesion day 65 occupied about 50% of the total width of the molecular layer. Immunoelectron microscopy localized L1 to the surface of unmyelinated axons in both normal and deafferented dentate gyrus. In situ hybridization revealed L1 messenger RNA confined to neurons throughout the hippocampal formation, but did not indicate changes in L1 messenger RNA levels in the hippocampus, dentate gyrus, entorhinal cortex or basal forebrain in response to unilateral entorhinal cortex lesions. Changes in L1 immunolabeling in the deafferented dentate gyrus corresponded in a spatial and temporal manner to changes of the synaptic marker synaptophysin and axonal marker phosphorylated tau. Results of the present study are most consistent with the view that L1 is expressed on reinnervating fibers after they make synaptic contacts with other structures. Thus, L1 appears to be involved in the maturation and stabilization of reinnervating fibers and consequently may play an important role in the repair process of the lesioned adult CNS.

AB - Expression of the neural adhesion molecule L1 and its potential involvement in axonal sprouting were examined in the deafferented rat dentate gyrus. We focused on the dentate gyrus because of its well-defined cytoarchitecture and well-characterized neuronal degeneration and sprouting response following entorhinal cortex lesions. In the molecular layer of the dentate gyrus, a trilaminar staining pattern was observed, with the middle molecular layer exhibiting slightly denser immunolabeling compared to both inner and outer molecular layers. Two to 12 days after a unilateral entorhinal cortex lesion, a progressive loss of L1 immunolabeling was noted in the ipsilateral middle and outer molecular layers, followed by a substantial reappearance of immunostaining 65 days after lesion incidence. The width of the immunostained ipsilateral inner molecular layer revealed a progressive widening and by postlesion day 65 occupied about 50% of the total width of the molecular layer. Immunoelectron microscopy localized L1 to the surface of unmyelinated axons in both normal and deafferented dentate gyrus. In situ hybridization revealed L1 messenger RNA confined to neurons throughout the hippocampal formation, but did not indicate changes in L1 messenger RNA levels in the hippocampus, dentate gyrus, entorhinal cortex or basal forebrain in response to unilateral entorhinal cortex lesions. Changes in L1 immunolabeling in the deafferented dentate gyrus corresponded in a spatial and temporal manner to changes of the synaptic marker synaptophysin and axonal marker phosphorylated tau. Results of the present study are most consistent with the view that L1 is expressed on reinnervating fibers after they make synaptic contacts with other structures. Thus, L1 appears to be involved in the maturation and stabilization of reinnervating fibers and consequently may play an important role in the repair process of the lesioned adult CNS.

KW - Animals

KW - Cell Adhesion Molecules, Neuronal

KW - Cholinergic Fibers

KW - Dentate Gyrus

KW - Hippocampus

KW - Immunohistochemistry

KW - In Situ Hybridization

KW - Male

KW - Rats

KW - Rats, Sprague-Dawley

KW - Journal Article

M3 - SCORING: Journal article

C2 - 8951867

VL - 75

SP - 703

EP - 715

JO - NEUROSCIENCE

JF - NEUROSCIENCE

SN - 0306-4522

IS - 3

ER -