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Neuronal counts of sensory ganglia in the\n                    <jats:italic>trkC<\/jats:italic>\n                    mutant mice reveal less severe losses than those in\n                    <jats:italic>NT-3<\/jats:italic>\n                    null mutant mice, strongly suggesting that\n                    <jats:italic>NT-3<\/jats:italic>\n                    ,\n                    <jats:italic>in vivo<\/jats:italic>\n                    , may signal through receptors other than\n                    <jats:italic>trkC<\/jats:italic>\n                    . Mice lacking either\n                    <jats:italic>NT-3<\/jats:italic>\n                    or all\n                    <jats:italic>trkC<\/jats:italic>\n                    receptor isoforms die in the early postnatal period. Histological examination of\n                    <jats:italic>trkC<\/jats:italic>\n                    -deficient mice reveals severe cardiac defects such as atrial and ventricular septal defects, and valvular defects including pulmonic stenosis. Formation of these structures during development is dependent on cardiac neural crest function. The similarities in cardiac defects observed in the\n                    <jats:italic>trkC<\/jats:italic>\n                    and\n                    <jats:italic>NT-3<\/jats:italic>\n                    null mutant mice indicate that the\n                    <jats:italic>trkC<\/jats:italic>\n                    receptor mediates most\n                    <jats:italic>NT-3<\/jats:italic>\n                    effects on the cardiac neural crest.\n                  <\/jats:p>","DOI":"10.1073\/pnas.94.26.14776","type":"journal-article","created":{"date-parts":[[2002,7,26]],"date-time":"2002-07-26T10:31:39Z","timestamp":1027679499000},"page":"14776-14781","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":176,"title":["Targeted deletion of all isoforms of the\n                    <i>trkC<\/i>\n                    gene suggests the use of alternate receptors by its ligand neurotrophin-3 in neuronal development and implicates\n           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