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Acetylcholinesterase-transgenic mice display embryonic modulations in spinal cord choline acetyltransferase and neurexin Iβ gene expression followed by late-onset neuromotor deterioration
Year:
1997
Authors :
Shani, Moshe
;
.
Volume :
94
Co-Authors:
Andres, C., Department of Biological Chemistry, Hebrew University of Jerusalem, 91904, Israel, Lab. de Biochim. et de Biol. Molec., Ctr. Hosp. Reg. Universitaire, INSERM U 316, 37044 Tours Cedex, France
Beeri, R., Department of Biological Chemistry, Hebrew University of Jerusalem, 91904, Israel
Friedman, A., Department of Biological Chemistry, Hebrew University of Jerusalem, 91904, Israel, Smith Foundation for Psychology
Lev-Lehman, E., Department of Biological Chemistry, Hebrew University of Jerusalem, 91904, Israel
Henis, S., Department of Biological Chemistry, Hebrew University of Jerusalem, 91904, Israel
Timberg, R., Department of Biological Chemistry, Hebrew University of Jerusalem, 91904, Israel
Shani, M., Department of Molecular Genetics, Agricultural Research Organization, Volcani Center, Bet Dagan, 50250, Israel
Soreq, H., Department of Biological Chemistry, Hebrew University of Jerusalem, 91904, Israel
Facilitators :
From page:
8173
To page:
8178
(
Total pages:
6
)
Abstract:
To explore the possibility that overproduction of neuronal acetylcholinesterase (AChE) confers changes in both cholinergic and morphogenic intercellular interactions, we studied developmental responses to neuronal AChE overexpression in motoneurons and neuromuscular junctions of AChE-transgenic mice. Perikarya of spinal cord motoneurons were consistently enlarged from embryonic through adult stages in AChE-transgenic mice. Atypical motoneuron development was accompanied by premature enhancement in the embryonic spinal cord expression of choline acetyltransferase mRNA, encoding the acetylcholine-synthesizing enzyme choline acetyltransferase. In contrast, the mRNA encoding for neurexin-1β, the heterophilic ligand of the AChE-homologous neuronal cell surface protein neuroligin, was drastically lower in embryonic transgenic spinal cord than in controls. Postnatal cessation of these dual transcriptional responses was followed by late-onset deterioration in neuromotor performance that was associated with gross aberrations in neuromuscular ultrastructure and with pronounced amyotrophy. These findings demonstrate embryonic feedback mechanisms to neuronal AChE overexpression that are attributable to both cholinergic and cell-cell interaction pathways, suggesting that embryonic neurexin Iβ expression is concerted in vivo with AChE levels and indicating that postnatal changes in neuronal AChE-associated proteins may be involved in late-onset neuromotor pathologies.
Note:
Related Files :
Acetylcholinesterase
animal experiment
Animals
animal tissue
gene expression
mice
Motoneurons
neuromuscular synapse
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More details
DOI :
10.1073/pnas.94.15.8173
Article number:
Affiliations:
Database:
Scopus
Publication Type:
article
;
.
Language:
English
Editors' remarks:
ID:
32054
Last updated date:
02/03/2022 17:27
Creation date:
17/04/2018 01:07
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Scientific Publication
Acetylcholinesterase-transgenic mice display embryonic modulations in spinal cord choline acetyltransferase and neurexin Iβ gene expression followed by late-onset neuromotor deterioration
94
Andres, C., Department of Biological Chemistry, Hebrew University of Jerusalem, 91904, Israel, Lab. de Biochim. et de Biol. Molec., Ctr. Hosp. Reg. Universitaire, INSERM U 316, 37044 Tours Cedex, France
Beeri, R., Department of Biological Chemistry, Hebrew University of Jerusalem, 91904, Israel
Friedman, A., Department of Biological Chemistry, Hebrew University of Jerusalem, 91904, Israel, Smith Foundation for Psychology
Lev-Lehman, E., Department of Biological Chemistry, Hebrew University of Jerusalem, 91904, Israel
Henis, S., Department of Biological Chemistry, Hebrew University of Jerusalem, 91904, Israel
Timberg, R., Department of Biological Chemistry, Hebrew University of Jerusalem, 91904, Israel
Shani, M., Department of Molecular Genetics, Agricultural Research Organization, Volcani Center, Bet Dagan, 50250, Israel
Soreq, H., Department of Biological Chemistry, Hebrew University of Jerusalem, 91904, Israel
Acetylcholinesterase-transgenic mice display embryonic modulations in spinal cord choline acetyltransferase and neurexin Iβ gene expression followed by late-onset neuromotor deterioration
To explore the possibility that overproduction of neuronal acetylcholinesterase (AChE) confers changes in both cholinergic and morphogenic intercellular interactions, we studied developmental responses to neuronal AChE overexpression in motoneurons and neuromuscular junctions of AChE-transgenic mice. Perikarya of spinal cord motoneurons were consistently enlarged from embryonic through adult stages in AChE-transgenic mice. Atypical motoneuron development was accompanied by premature enhancement in the embryonic spinal cord expression of choline acetyltransferase mRNA, encoding the acetylcholine-synthesizing enzyme choline acetyltransferase. In contrast, the mRNA encoding for neurexin-1β, the heterophilic ligand of the AChE-homologous neuronal cell surface protein neuroligin, was drastically lower in embryonic transgenic spinal cord than in controls. Postnatal cessation of these dual transcriptional responses was followed by late-onset deterioration in neuromotor performance that was associated with gross aberrations in neuromuscular ultrastructure and with pronounced amyotrophy. These findings demonstrate embryonic feedback mechanisms to neuronal AChE overexpression that are attributable to both cholinergic and cell-cell interaction pathways, suggesting that embryonic neurexin Iβ expression is concerted in vivo with AChE levels and indicating that postnatal changes in neuronal AChE-associated proteins may be involved in late-onset neuromotor pathologies.
Scientific Publication
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