Subcellular Localization of Intercellular Adhesion Molecule-5 (Telencephalin) in the Visual Cortex Is Not Developmentally Regulated in the Absence of Matrix Metalloproteinase-9. Kelly, E. A., Tremblay, M., Gahmberg, C. G., Tian, L., & Majewska, A. K. Journal of Comparative Neurology, 522(3):676–688, February, 2014. WOS:000328656300011doi abstract bibtex The telencephalon-associated intercellular adhesion molecule-5 (telencephalin; ICAM-5) regulates dendritic morphology in the developing brain. In vitro studies have shown that ICAM-5 is found predominantly within dendrites and immature dendritic protrusions, with reduced expression in mushroom spines, suggesting that ICAM-5 downregulation is critical for the maturation of synaptic structures. However, developmental expression of ICAM-5 has not been explored in depth at the ultrastructural level in intact brain tissue. To investigate the ultrastructural localization of ICAM-5 with transmission electron microscopy, we performed immunoperoxidase histochemistry for ICAM-5 in mouse visual cortex at postnatal day (P)14, a period of intense synaptogenesis, and at P28, when synapses mature. We observed the expected ICAM-5 expression in dendritic protrusions and shafts at both P14 and P28. ICAM-5 expression in these dendritic protrusions decreased in prevalence with developmental age to become localized predominantly to dendritic shafts by P28. To understand better the relationship between ICAM-5 and the endopeptidase metalloproteinase-9 (MMP-9), which mediates ICAM-5 cleavage following glutamate activation during postnatal development, we also explored ICAM-5 expression in MMP-9 null animals. This analysis revealed a similar expression of ICAM-5 in dendritic elements at P14 and P28; however, an increased prevalence of ICAM-5 was noted in dendritic protrusions at P28 in the MMP-9 null animals, indicating that, in the absence of MMP-9, there is no developmental shift in ICAM-5 subcellular localization. Our ultrastructural observations shed light on possible functions mediated by ICAM-5 and their regulation by extracellular proteases. J. Comp. Neurol. 522:676-688, 2013. (c) 2013 Wiley Periodicals, Inc.
@article{kelly_subcellular_2014,
title = {Subcellular {Localization} of {Intercellular} {Adhesion} {Molecule}-5 ({Telencephalin}) in the {Visual} {Cortex} {Is} {Not} {Developmentally} {Regulated} in the {Absence} of {Matrix} {Metalloproteinase}-9},
volume = {522},
issn = {0021-9967},
doi = {10.1002/cne.23440},
abstract = {The telencephalon-associated intercellular adhesion molecule-5 (telencephalin; ICAM-5) regulates dendritic morphology in the developing brain. In vitro studies have shown that ICAM-5 is found predominantly within dendrites and immature dendritic protrusions, with reduced expression in mushroom spines, suggesting that ICAM-5 downregulation is critical for the maturation of synaptic structures. However, developmental expression of ICAM-5 has not been explored in depth at the ultrastructural level in intact brain tissue. To investigate the ultrastructural localization of ICAM-5 with transmission electron microscopy, we performed immunoperoxidase histochemistry for ICAM-5 in mouse visual cortex at postnatal day (P)14, a period of intense synaptogenesis, and at P28, when synapses mature. We observed the expected ICAM-5 expression in dendritic protrusions and shafts at both P14 and P28. ICAM-5 expression in these dendritic protrusions decreased in prevalence with developmental age to become localized predominantly to dendritic shafts by P28. To understand better the relationship between ICAM-5 and the endopeptidase metalloproteinase-9 (MMP-9), which mediates ICAM-5 cleavage following glutamate activation during postnatal development, we also explored ICAM-5 expression in MMP-9 null animals. This analysis revealed a similar expression of ICAM-5 in dendritic elements at P14 and P28; however, an increased prevalence of ICAM-5 was noted in dendritic protrusions at P28 in the MMP-9 null animals, indicating that, in the absence of MMP-9, there is no developmental shift in ICAM-5 subcellular localization. Our ultrastructural observations shed light on possible functions mediated by ICAM-5 and their regulation by extracellular proteases. J. Comp. Neurol. 522:676-688, 2013. (c) 2013 Wiley Periodicals, Inc.},
language = {English},
number = {3},
journal = {Journal of Comparative Neurology},
author = {Kelly, Emily A. and Tremblay, Marie-Eve and Gahmberg, Carl G. and Tian, Li and Majewska, Ania K.},
month = feb,
year = {2014},
note = {WOS:000328656300011},
keywords = {Electron microscopy, brain, dendrite, epha4, expression, icam-5, leukocyte adhesion, long-term potentiation, matrix metalloproteinases, membrane glycoprotein, microglia, mmp-9, neuronal glycoprotein, plasticity, rat hippocampus, telencephalin},
pages = {676--688},
}
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In vitro studies have shown that ICAM-5 is found predominantly within dendrites and immature dendritic protrusions, with reduced expression in mushroom spines, suggesting that ICAM-5 downregulation is critical for the maturation of synaptic structures. However, developmental expression of ICAM-5 has not been explored in depth at the ultrastructural level in intact brain tissue. To investigate the ultrastructural localization of ICAM-5 with transmission electron microscopy, we performed immunoperoxidase histochemistry for ICAM-5 in mouse visual cortex at postnatal day (P)14, a period of intense synaptogenesis, and at P28, when synapses mature. We observed the expected ICAM-5 expression in dendritic protrusions and shafts at both P14 and P28. ICAM-5 expression in these dendritic protrusions decreased in prevalence with developmental age to become localized predominantly to dendritic shafts by P28. To understand better the relationship between ICAM-5 and the endopeptidase metalloproteinase-9 (MMP-9), which mediates ICAM-5 cleavage following glutamate activation during postnatal development, we also explored ICAM-5 expression in MMP-9 null animals. This analysis revealed a similar expression of ICAM-5 in dendritic elements at P14 and P28; however, an increased prevalence of ICAM-5 was noted in dendritic protrusions at P28 in the MMP-9 null animals, indicating that, in the absence of MMP-9, there is no developmental shift in ICAM-5 subcellular localization. Our ultrastructural observations shed light on possible functions mediated by ICAM-5 and their regulation by extracellular proteases. J. Comp. Neurol. 522:676-688, 2013. 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