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Antigen recognized by monoclonal antibodies to mesencephalic neural crest and to ciliary ganglion neurons is involved in the high affinity choline uptake mechanism in these cells

dc.contributor.authorBarald, Kate F.en_US
dc.date.accessioned2007-04-06T18:40:17Z
dc.date.available2007-04-06T18:40:17Z
dc.date.issued1988-10en_US
dc.identifier.citationBarald, Kate F. (1988)."Antigen recognized by monoclonal antibodies to mesencephalic neural crest and to ciliary ganglion neurons is involved in the high affinity choline uptake mechanism in these cells." Journal of Neuroscience Research 21(2-4): 119-134. <http://hdl.handle.net/2027.42/50220>en_US
dc.identifier.issn0360-4012en_US
dc.identifier.issn1097-4547en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/50220
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=3216416&dopt=citationen_US
dc.description.abstractHigh-affinity choline uptake mechanisms are among the characteristics of cholinergic neurons such as the ciliary and choroid subpopulations in the ciliary ganglion (Barald and Berg, 1979). We have produced three monoclonal antibodies (Mabs), two of which were made to 8-day embryonic chick ciliary ganglion (CG) neurons (CG-1, CG-4) (Barald, 1982) and one of which was made to cultured mesencephalic neural crest (NC) cells (CG-14) removed from the embryo 31 hr after incubation. We have shown that all three Mabs label a common 75 kD antigen present on the cell surface of both CG neurons and NC cells (Barald, 1988). Here we report that the CG-1 and CG-4 antibodies, used in the same ratios in which they are synergistically cytotoxic for both the CG and NC cells (Barald, 1988), and Mab CG-14 alone, have specific effects on the high-affinity choline uptake mechanism (HACU) of CG neurons and isolated antigen-positive NC cells in the absence of complement. CG-1 and CG-4 in ratios of 8/1 (the same ratios that are used to kill the CG and the NC subpopulation), but neither singly, inhibit the HACU of CG neurons by 40% and that of isolated antigen-positive NC cells by 75%. However, CG-14 alone, at 1 Μg/ml, inhibits the HACU of both CG neurons and isolated NC cells by 95%. None of the antibodies had an effect on numbers of ouabain binding sites (a measure of the Na + /K + ATPase) or cell surface acetylcholinesterase (AChE) of CG neurons or NC cells isolated by “no-flow” fluorescence cytometry with a Meridian Instruments ACAS470 cytometer. CG or NC cells grown in the presence of the antibodies without complement grow and remain healthy for many weeks. They exhibit no difference in morphology, protein content, lactate dehydrogenase activity (LDH), or division time from untreated sister cultures. Therefore, the antigen recognized by all three Mabs may be involved in a high-affinity choline uptake mechanism, a common characteristic of cholinergic neurons. The Mabs themselves may possibly label some element of the high-affinity transporter or a proximal membrane component. This implies that such a high-affinity uptake mechanism is present in the subpopulation of NC cells at early times in development. If these cells in fact are destined to contribute to the avian CG, these characteristics are present in the subpopulation before the NC cells take on a neuronal morphology.en_US
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dc.format.extent3118 bytes
dc.format.mimetypeapplication/pdf
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dc.publisherWiley Subscription Services, Inc., A Wiley Companyen_US
dc.subject.otherLife and Medical Sciencesen_US
dc.subject.otherNeuroscience, Neurology and Psychiatryen_US
dc.titleAntigen recognized by monoclonal antibodies to mesencephalic neural crest and to ciliary ganglion neurons is involved in the high affinity choline uptake mechanism in these cellsen_US
dc.typeArticleen_US
dc.rights.robotsIndexNoFollowen_US
dc.subject.hlbsecondlevelMolecular, Cellular and Developmental Biologyen_US
dc.subject.hlbsecondlevelNeurosciencesen_US
dc.subject.hlbsecondlevelPsychologyen_US
dc.subject.hlbsecondlevelPublic Healthen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.subject.hlbtoplevelScienceen_US
dc.subject.hlbtoplevelSocial Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumDepartment of Anatomy and Cell Biology, Program in Neuroscience, Program in Cell and Molecular Biology, University of Michigan Medical School, Ann Arbor ; Department of Anatomy and Cell Biology, University of Michigan, Box 0616, Ann Arbor, MI 48109en_US
dc.identifier.pmid3216416en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/50220/1/490210205_ftp.pdfen_US
dc.identifier.doihttp://dx.doi.org/10.1002/jnr.490210205en_US
dc.identifier.sourceJournal of Neuroscience Researchen_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


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