CRITICAL ROLES FOR THE NETRIN RECEPTOR DELETED IN COLORECTAL CANCER IN DOPAMINERGIC NEURONAL PRECURSOR MIGRATION, AXON GUIDANCE, AND AXON ARBORIZATION
Identifieur interne : 000405 ( PascalFrancis/Corpus ); précédent : 000404; suivant : 000406CRITICAL ROLES FOR THE NETRIN RECEPTOR DELETED IN COLORECTAL CANCER IN DOPAMINERGIC NEURONAL PRECURSOR MIGRATION, AXON GUIDANCE, AND AXON ARBORIZATION
Auteurs : B. Xu ; J. S. Goldman ; V. V. Rymar ; C. Forget ; P. S. Lo ; S. J. Bull ; E. Vereker ; P. A. Barker ; L. E. Trudeau ; A. F. Sadikot ; T. E. KennedySource :
- Neuroscience [ 0306-4522 ] ; 2010.
Descripteurs français
- Pascal (Inist)
English descriptors
Abstract
DCC (deleted in colorectal cancer), a receptor for the axon guidance cue netrin-1, is highly expressed by mesencephalic dopaminergic (DA) neurons during development; however, the contribution of DCC to DA development remains largely uncharacterized. DA neurons in ventral mesencephalic nuclei also express UNC5 homologue netrin receptors from late embryogenesis to adulthood, raising the possibility that DA axons could be attracted or repelled by netrins. Examining newborn dcc null mice, we report that loss of DCC function results in profound alterations of DA circuitry, including DA progenitor cell migration defects, reduced numbers of DA cells in midbrain nuclei, an anomalous DA ventral commissure, malformed DA innervation of the ventral striatum, and reduced DA innervation of the cerebral cortex. Caspase-3 activation was detected in inappropriately localized DA cells, consistent with apoptosis contributing to reduced cell numbers. Dcc heterozygous mice express reduced levels of DCC protein. Although less severely disrupted than dcc nulls, newborn and adult dcc heterozygotes also have fewer DA neurons in ventral mesenscephalic nuclei. Despite the reduced numbers of DA neurons, newborn dcc heterozygotes and nulls exhibit similar DA innervation density as wild-type littermates in the nucleus accumbens core, and adult dcc heterozygotes exhibit increased DA innervation in medial prefrontal cortex. A trend towards increased innervation of medial prefrontal cortex was detected in newborn dcc heterozygotes, but did not reach statistical significance, suggesting that the increase in adult heterozygotes results from enhanced DA arborization during postnatal development. Consistent with the hypothesis that DCC regulates DA axonal projections, disrupting DCC function in culture inhibits netrin-1 induced DA axon extension and axon branching. Furthermore, disrupting DCC function in isolated DA neurons grown as micro-island cultures reduces the number of autaptic synapses per cell. We conclude that DCC regulates appropriate precursor cell migration, axon guidance, and terminal arborization by DA neurons.
Notice en format standard (ISO 2709)
Pour connaître la documentation sur le format Inist Standard.
pA |
|
---|
Format Inist (serveur)
NO : | PASCAL 10-0397347 INIST |
---|---|
ET : | CRITICAL ROLES FOR THE NETRIN RECEPTOR DELETED IN COLORECTAL CANCER IN DOPAMINERGIC NEURONAL PRECURSOR MIGRATION, AXON GUIDANCE, AND AXON ARBORIZATION |
AU : | XU (B.); GOLDMAN (J. S.); RYMAR (V. V.); FORGET (C.); LO (P. S.); BULL (S. J.); VEREKER (E.); BARKER (P. A.); TRUDEAU (L. E.); SADIKOT (A. F.); KENNEDY (T. E.) |
AF : | Centre for Neuronal Survival, Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University/Montreal, QC, H3A 2B4/Canada (1 aut., 2 aut., 5 aut., 6 aut., 7 aut., 8 aut., 11 aut.); Cone Laboratory, Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University/Montreal, QC, H3A 2B4/Canada (3 aut., 5 aut., 10 aut.); Département de Pharmacologie, Faculté de Médecine, Université de Montréal/Montréal, QC, H3C 3J7/Canada (4 aut., 9 aut.) |
DT : | Publication en série; Niveau analytique |
SO : | Neuroscience; ISSN 0306-4522; Coden NRSCDN; Pays-Bas; Da. 2010; Vol. 169; No. 2; Pp. 932-949; Bibl. 1 p. |
LA : | Anglais |
EA : | DCC (deleted in colorectal cancer), a receptor for the axon guidance cue netrin-1, is highly expressed by mesencephalic dopaminergic (DA) neurons during development; however, the contribution of DCC to DA development remains largely uncharacterized. DA neurons in ventral mesencephalic nuclei also express UNC5 homologue netrin receptors from late embryogenesis to adulthood, raising the possibility that DA axons could be attracted or repelled by netrins. Examining newborn dcc null mice, we report that loss of DCC function results in profound alterations of DA circuitry, including DA progenitor cell migration defects, reduced numbers of DA cells in midbrain nuclei, an anomalous DA ventral commissure, malformed DA innervation of the ventral striatum, and reduced DA innervation of the cerebral cortex. Caspase-3 activation was detected in inappropriately localized DA cells, consistent with apoptosis contributing to reduced cell numbers. Dcc heterozygous mice express reduced levels of DCC protein. Although less severely disrupted than dcc nulls, newborn and adult dcc heterozygotes also have fewer DA neurons in ventral mesenscephalic nuclei. Despite the reduced numbers of DA neurons, newborn dcc heterozygotes and nulls exhibit similar DA innervation density as wild-type littermates in the nucleus accumbens core, and adult dcc heterozygotes exhibit increased DA innervation in medial prefrontal cortex. A trend towards increased innervation of medial prefrontal cortex was detected in newborn dcc heterozygotes, but did not reach statistical significance, suggesting that the increase in adult heterozygotes results from enhanced DA arborization during postnatal development. Consistent with the hypothesis that DCC regulates DA axonal projections, disrupting DCC function in culture inhibits netrin-1 induced DA axon extension and axon branching. Furthermore, disrupting DCC function in isolated DA neurons grown as micro-island cultures reduces the number of autaptic synapses per cell. We conclude that DCC regulates appropriate precursor cell migration, axon guidance, and terminal arborization by DA neurons. |
CC : | 002A25; 002B17G |
FD : | Récepteur biologique; Dopamine; Axone; Synaptogenèse; Maladie de Parkinson; Schizophrénie |
FG : | Catécholamine; Neurotransmetteur; Maladie dégénérative; Pathologie du système nerveux; Pathologie de l'encéphale; Syndrome extrapyramidal; Pathologie du système nerveux central; Psychose |
ED : | Biological receptor; Dopamine; Axon; Synaptogenesis; Parkinson disease; Schizophrenia |
EG : | Catecholamine; Neurotransmitter; Degenerative disease; Nervous system diseases; Cerebral disorder; Extrapyramidal syndrome; Central nervous system disease; Psychosis |
SD : | Receptor biológico; Dopamina; Axón; Sinaptogénesis; Parkinson enfermedad; Esquizofrenia |
LO : | INIST-17194.354000194123870350 |
ID : | 10-0397347 |
Links to Exploration step
Pascal:10-0397347Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en" level="a">CRITICAL ROLES FOR THE NETRIN RECEPTOR DELETED IN COLORECTAL CANCER IN DOPAMINERGIC NEURONAL PRECURSOR MIGRATION, AXON GUIDANCE, AND AXON ARBORIZATION</title>
<author><name sortKey="Xu, B" sort="Xu, B" uniqKey="Xu B" first="B." last="Xu">B. Xu</name>
<affiliation><inist:fA14 i1="01"><s1>Centre for Neuronal Survival, Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University</s1>
<s2>Montreal, QC, H3A 2B4</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>11 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Goldman, J S" sort="Goldman, J S" uniqKey="Goldman J" first="J. S." last="Goldman">J. S. Goldman</name>
<affiliation><inist:fA14 i1="01"><s1>Centre for Neuronal Survival, Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University</s1>
<s2>Montreal, QC, H3A 2B4</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>11 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Rymar, V V" sort="Rymar, V V" uniqKey="Rymar V" first="V. V." last="Rymar">V. V. Rymar</name>
<affiliation><inist:fA14 i1="02"><s1>Cone Laboratory, Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University</s1>
<s2>Montreal, QC, H3A 2B4</s2>
<s3>CAN</s3>
<sZ>3 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>10 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Forget, C" sort="Forget, C" uniqKey="Forget C" first="C." last="Forget">C. Forget</name>
<affiliation><inist:fA14 i1="03"><s1>Département de Pharmacologie, Faculté de Médecine, Université de Montréal</s1>
<s2>Montréal, QC, H3C 3J7</s2>
<s3>CAN</s3>
<sZ>4 aut.</sZ>
<sZ>9 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Lo, P S" sort="Lo, P S" uniqKey="Lo P" first="P. S." last="Lo">P. S. Lo</name>
<affiliation><inist:fA14 i1="01"><s1>Centre for Neuronal Survival, Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University</s1>
<s2>Montreal, QC, H3A 2B4</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>11 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="02"><s1>Cone Laboratory, Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University</s1>
<s2>Montreal, QC, H3A 2B4</s2>
<s3>CAN</s3>
<sZ>3 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>10 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Bull, S J" sort="Bull, S J" uniqKey="Bull S" first="S. J." last="Bull">S. J. Bull</name>
<affiliation><inist:fA14 i1="01"><s1>Centre for Neuronal Survival, Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University</s1>
<s2>Montreal, QC, H3A 2B4</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>11 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Vereker, E" sort="Vereker, E" uniqKey="Vereker E" first="E." last="Vereker">E. Vereker</name>
<affiliation><inist:fA14 i1="01"><s1>Centre for Neuronal Survival, Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University</s1>
<s2>Montreal, QC, H3A 2B4</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>11 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Barker, P A" sort="Barker, P A" uniqKey="Barker P" first="P. A." last="Barker">P. A. Barker</name>
<affiliation><inist:fA14 i1="01"><s1>Centre for Neuronal Survival, Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University</s1>
<s2>Montreal, QC, H3A 2B4</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>11 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Trudeau, L E" sort="Trudeau, L E" uniqKey="Trudeau L" first="L. E." last="Trudeau">L. E. Trudeau</name>
<affiliation><inist:fA14 i1="03"><s1>Département de Pharmacologie, Faculté de Médecine, Université de Montréal</s1>
<s2>Montréal, QC, H3C 3J7</s2>
<s3>CAN</s3>
<sZ>4 aut.</sZ>
<sZ>9 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Sadikot, A F" sort="Sadikot, A F" uniqKey="Sadikot A" first="A. F." last="Sadikot">A. F. Sadikot</name>
<affiliation><inist:fA14 i1="02"><s1>Cone Laboratory, Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University</s1>
<s2>Montreal, QC, H3A 2B4</s2>
<s3>CAN</s3>
<sZ>3 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>10 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Kennedy, T E" sort="Kennedy, T E" uniqKey="Kennedy T" first="T. E." last="Kennedy">T. E. Kennedy</name>
<affiliation><inist:fA14 i1="01"><s1>Centre for Neuronal Survival, Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University</s1>
<s2>Montreal, QC, H3A 2B4</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>11 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">INIST</idno>
<idno type="inist">10-0397347</idno>
<date when="2010">2010</date>
<idno type="stanalyst">PASCAL 10-0397347 INIST</idno>
<idno type="RBID">Pascal:10-0397347</idno>
<idno type="wicri:Area/PascalFrancis/Corpus">000405</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">CRITICAL ROLES FOR THE NETRIN RECEPTOR DELETED IN COLORECTAL CANCER IN DOPAMINERGIC NEURONAL PRECURSOR MIGRATION, AXON GUIDANCE, AND AXON ARBORIZATION</title>
<author><name sortKey="Xu, B" sort="Xu, B" uniqKey="Xu B" first="B." last="Xu">B. Xu</name>
<affiliation><inist:fA14 i1="01"><s1>Centre for Neuronal Survival, Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University</s1>
<s2>Montreal, QC, H3A 2B4</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>11 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Goldman, J S" sort="Goldman, J S" uniqKey="Goldman J" first="J. S." last="Goldman">J. S. Goldman</name>
<affiliation><inist:fA14 i1="01"><s1>Centre for Neuronal Survival, Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University</s1>
<s2>Montreal, QC, H3A 2B4</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>11 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Rymar, V V" sort="Rymar, V V" uniqKey="Rymar V" first="V. V." last="Rymar">V. V. Rymar</name>
<affiliation><inist:fA14 i1="02"><s1>Cone Laboratory, Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University</s1>
<s2>Montreal, QC, H3A 2B4</s2>
<s3>CAN</s3>
<sZ>3 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>10 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Forget, C" sort="Forget, C" uniqKey="Forget C" first="C." last="Forget">C. Forget</name>
<affiliation><inist:fA14 i1="03"><s1>Département de Pharmacologie, Faculté de Médecine, Université de Montréal</s1>
<s2>Montréal, QC, H3C 3J7</s2>
<s3>CAN</s3>
<sZ>4 aut.</sZ>
<sZ>9 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Lo, P S" sort="Lo, P S" uniqKey="Lo P" first="P. S." last="Lo">P. S. Lo</name>
<affiliation><inist:fA14 i1="01"><s1>Centre for Neuronal Survival, Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University</s1>
<s2>Montreal, QC, H3A 2B4</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>11 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="02"><s1>Cone Laboratory, Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University</s1>
<s2>Montreal, QC, H3A 2B4</s2>
<s3>CAN</s3>
<sZ>3 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>10 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Bull, S J" sort="Bull, S J" uniqKey="Bull S" first="S. J." last="Bull">S. J. Bull</name>
<affiliation><inist:fA14 i1="01"><s1>Centre for Neuronal Survival, Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University</s1>
<s2>Montreal, QC, H3A 2B4</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>11 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Vereker, E" sort="Vereker, E" uniqKey="Vereker E" first="E." last="Vereker">E. Vereker</name>
<affiliation><inist:fA14 i1="01"><s1>Centre for Neuronal Survival, Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University</s1>
<s2>Montreal, QC, H3A 2B4</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>11 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Barker, P A" sort="Barker, P A" uniqKey="Barker P" first="P. A." last="Barker">P. A. Barker</name>
<affiliation><inist:fA14 i1="01"><s1>Centre for Neuronal Survival, Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University</s1>
<s2>Montreal, QC, H3A 2B4</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>11 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Trudeau, L E" sort="Trudeau, L E" uniqKey="Trudeau L" first="L. E." last="Trudeau">L. E. Trudeau</name>
<affiliation><inist:fA14 i1="03"><s1>Département de Pharmacologie, Faculté de Médecine, Université de Montréal</s1>
<s2>Montréal, QC, H3C 3J7</s2>
<s3>CAN</s3>
<sZ>4 aut.</sZ>
<sZ>9 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Sadikot, A F" sort="Sadikot, A F" uniqKey="Sadikot A" first="A. F." last="Sadikot">A. F. Sadikot</name>
<affiliation><inist:fA14 i1="02"><s1>Cone Laboratory, Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University</s1>
<s2>Montreal, QC, H3A 2B4</s2>
<s3>CAN</s3>
<sZ>3 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>10 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Kennedy, T E" sort="Kennedy, T E" uniqKey="Kennedy T" first="T. E." last="Kennedy">T. E. Kennedy</name>
<affiliation><inist:fA14 i1="01"><s1>Centre for Neuronal Survival, Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University</s1>
<s2>Montreal, QC, H3A 2B4</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>11 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
</analytic>
<series><title level="j" type="main">Neuroscience</title>
<title level="j" type="abbreviated">Neuroscience</title>
<idno type="ISSN">0306-4522</idno>
<imprint><date when="2010">2010</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
<seriesStmt><title level="j" type="main">Neuroscience</title>
<title level="j" type="abbreviated">Neuroscience</title>
<idno type="ISSN">0306-4522</idno>
</seriesStmt>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Axon</term>
<term>Biological receptor</term>
<term>Dopamine</term>
<term>Parkinson disease</term>
<term>Schizophrenia</term>
<term>Synaptogenesis</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Récepteur biologique</term>
<term>Dopamine</term>
<term>Axone</term>
<term>Synaptogenèse</term>
<term>Maladie de Parkinson</term>
<term>Schizophrénie</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">DCC (deleted in colorectal cancer), a receptor for the axon guidance cue netrin-1, is highly expressed by mesencephalic dopaminergic (DA) neurons during development; however, the contribution of DCC to DA development remains largely uncharacterized. DA neurons in ventral mesencephalic nuclei also express UNC5 homologue netrin receptors from late embryogenesis to adulthood, raising the possibility that DA axons could be attracted or repelled by netrins. Examining newborn dcc null mice, we report that loss of DCC function results in profound alterations of DA circuitry, including DA progenitor cell migration defects, reduced numbers of DA cells in midbrain nuclei, an anomalous DA ventral commissure, malformed DA innervation of the ventral striatum, and reduced DA innervation of the cerebral cortex. Caspase-3 activation was detected in inappropriately localized DA cells, consistent with apoptosis contributing to reduced cell numbers. Dcc heterozygous mice express reduced levels of DCC protein. Although less severely disrupted than dcc nulls, newborn and adult dcc heterozygotes also have fewer DA neurons in ventral mesenscephalic nuclei. Despite the reduced numbers of DA neurons, newborn dcc heterozygotes and nulls exhibit similar DA innervation density as wild-type littermates in the nucleus accumbens core, and adult dcc heterozygotes exhibit increased DA innervation in medial prefrontal cortex. A trend towards increased innervation of medial prefrontal cortex was detected in newborn dcc heterozygotes, but did not reach statistical significance, suggesting that the increase in adult heterozygotes results from enhanced DA arborization during postnatal development. Consistent with the hypothesis that DCC regulates DA axonal projections, disrupting DCC function in culture inhibits netrin-1 induced DA axon extension and axon branching. Furthermore, disrupting DCC function in isolated DA neurons grown as micro-island cultures reduces the number of autaptic synapses per cell. We conclude that DCC regulates appropriate precursor cell migration, axon guidance, and terminal arborization by DA neurons.</div>
</front>
</TEI>
<inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0306-4522</s0>
</fA01>
<fA02 i1="01"><s0>NRSCDN</s0>
</fA02>
<fA03 i2="1"><s0>Neuroscience</s0>
</fA03>
<fA05><s2>169</s2>
</fA05>
<fA06><s2>2</s2>
</fA06>
<fA08 i1="01" i2="1" l="ENG"><s1>CRITICAL ROLES FOR THE NETRIN RECEPTOR DELETED IN COLORECTAL CANCER IN DOPAMINERGIC NEURONAL PRECURSOR MIGRATION, AXON GUIDANCE, AND AXON ARBORIZATION</s1>
</fA08>
<fA11 i1="01" i2="1"><s1>XU (B.)</s1>
</fA11>
<fA11 i1="02" i2="1"><s1>GOLDMAN (J. S.)</s1>
</fA11>
<fA11 i1="03" i2="1"><s1>RYMAR (V. V.)</s1>
</fA11>
<fA11 i1="04" i2="1"><s1>FORGET (C.)</s1>
</fA11>
<fA11 i1="05" i2="1"><s1>LO (P. S.)</s1>
</fA11>
<fA11 i1="06" i2="1"><s1>BULL (S. J.)</s1>
</fA11>
<fA11 i1="07" i2="1"><s1>VEREKER (E.)</s1>
</fA11>
<fA11 i1="08" i2="1"><s1>BARKER (P. A.)</s1>
</fA11>
<fA11 i1="09" i2="1"><s1>TRUDEAU (L. E.)</s1>
</fA11>
<fA11 i1="10" i2="1"><s1>SADIKOT (A. F.)</s1>
</fA11>
<fA11 i1="11" i2="1"><s1>KENNEDY (T. E.)</s1>
</fA11>
<fA14 i1="01"><s1>Centre for Neuronal Survival, Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University</s1>
<s2>Montreal, QC, H3A 2B4</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>11 aut.</sZ>
</fA14>
<fA14 i1="02"><s1>Cone Laboratory, Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University</s1>
<s2>Montreal, QC, H3A 2B4</s2>
<s3>CAN</s3>
<sZ>3 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>10 aut.</sZ>
</fA14>
<fA14 i1="03"><s1>Département de Pharmacologie, Faculté de Médecine, Université de Montréal</s1>
<s2>Montréal, QC, H3C 3J7</s2>
<s3>CAN</s3>
<sZ>4 aut.</sZ>
<sZ>9 aut.</sZ>
</fA14>
<fA20><s1>932-949</s1>
</fA20>
<fA21><s1>2010</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
</fA23>
<fA43 i1="01"><s1>INIST</s1>
<s2>17194</s2>
<s5>354000194123870350</s5>
</fA43>
<fA44><s0>0000</s0>
<s1>© 2010 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45><s0>1 p.</s0>
</fA45>
<fA47 i1="01" i2="1"><s0>10-0397347</s0>
</fA47>
<fA60><s1>P</s1>
</fA60>
<fA61><s0>A</s0>
</fA61>
<fA64 i1="01" i2="1"><s0>Neuroscience</s0>
</fA64>
<fA66 i1="01"><s0>NLD</s0>
</fA66>
<fC01 i1="01" l="ENG"><s0>DCC (deleted in colorectal cancer), a receptor for the axon guidance cue netrin-1, is highly expressed by mesencephalic dopaminergic (DA) neurons during development; however, the contribution of DCC to DA development remains largely uncharacterized. DA neurons in ventral mesencephalic nuclei also express UNC5 homologue netrin receptors from late embryogenesis to adulthood, raising the possibility that DA axons could be attracted or repelled by netrins. Examining newborn dcc null mice, we report that loss of DCC function results in profound alterations of DA circuitry, including DA progenitor cell migration defects, reduced numbers of DA cells in midbrain nuclei, an anomalous DA ventral commissure, malformed DA innervation of the ventral striatum, and reduced DA innervation of the cerebral cortex. Caspase-3 activation was detected in inappropriately localized DA cells, consistent with apoptosis contributing to reduced cell numbers. Dcc heterozygous mice express reduced levels of DCC protein. Although less severely disrupted than dcc nulls, newborn and adult dcc heterozygotes also have fewer DA neurons in ventral mesenscephalic nuclei. Despite the reduced numbers of DA neurons, newborn dcc heterozygotes and nulls exhibit similar DA innervation density as wild-type littermates in the nucleus accumbens core, and adult dcc heterozygotes exhibit increased DA innervation in medial prefrontal cortex. A trend towards increased innervation of medial prefrontal cortex was detected in newborn dcc heterozygotes, but did not reach statistical significance, suggesting that the increase in adult heterozygotes results from enhanced DA arborization during postnatal development. Consistent with the hypothesis that DCC regulates DA axonal projections, disrupting DCC function in culture inhibits netrin-1 induced DA axon extension and axon branching. Furthermore, disrupting DCC function in isolated DA neurons grown as micro-island cultures reduces the number of autaptic synapses per cell. We conclude that DCC regulates appropriate precursor cell migration, axon guidance, and terminal arborization by DA neurons.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002A25</s0>
</fC02>
<fC02 i1="02" i2="X"><s0>002B17G</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Récepteur biologique</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Biological receptor</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Receptor biológico</s0>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Dopamine</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Dopamine</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Dopamina</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Axone</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Axon</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Axón</s0>
<s5>03</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Synaptogenèse</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Synaptogenesis</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Sinaptogénesis</s0>
<s5>04</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Maladie de Parkinson</s0>
<s2>NM</s2>
<s5>09</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Parkinson disease</s0>
<s2>NM</s2>
<s5>09</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Parkinson enfermedad</s0>
<s2>NM</s2>
<s5>09</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Schizophrénie</s0>
<s5>12</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Schizophrenia</s0>
<s5>12</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Esquizofrenia</s0>
<s5>12</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Catécholamine</s0>
<s5>20</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Catecholamine</s0>
<s5>20</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Catecolamina</s0>
<s5>20</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Neurotransmetteur</s0>
<s5>21</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Neurotransmitter</s0>
<s5>21</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Neurotransmisor</s0>
<s5>21</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Maladie dégénérative</s0>
<s5>22</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Degenerative disease</s0>
<s5>22</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>22</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Pathologie du système nerveux</s0>
<s5>23</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Nervous system diseases</s0>
<s5>23</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Sistema nervioso patología</s0>
<s5>23</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Pathologie de l'encéphale</s0>
<s5>24</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>24</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>24</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Syndrome extrapyramidal</s0>
<s5>25</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0>
<s5>25</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0>
<s5>25</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Pathologie du système nerveux central</s0>
<s5>26</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Central nervous system disease</s0>
<s5>26</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0>
<s5>26</s5>
</fC07>
<fC07 i1="08" i2="X" l="FRE"><s0>Psychose</s0>
<s5>27</s5>
</fC07>
<fC07 i1="08" i2="X" l="ENG"><s0>Psychosis</s0>
<s5>27</s5>
</fC07>
<fC07 i1="08" i2="X" l="SPA"><s0>Psicosis</s0>
<s5>27</s5>
</fC07>
<fN21><s1>256</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
</standard>
<server><NO>PASCAL 10-0397347 INIST</NO>
<ET>CRITICAL ROLES FOR THE NETRIN RECEPTOR DELETED IN COLORECTAL CANCER IN DOPAMINERGIC NEURONAL PRECURSOR MIGRATION, AXON GUIDANCE, AND AXON ARBORIZATION</ET>
<AU>XU (B.); GOLDMAN (J. S.); RYMAR (V. V.); FORGET (C.); LO (P. S.); BULL (S. J.); VEREKER (E.); BARKER (P. A.); TRUDEAU (L. E.); SADIKOT (A. F.); KENNEDY (T. E.)</AU>
<AF>Centre for Neuronal Survival, Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University/Montreal, QC, H3A 2B4/Canada (1 aut., 2 aut., 5 aut., 6 aut., 7 aut., 8 aut., 11 aut.); Cone Laboratory, Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University/Montreal, QC, H3A 2B4/Canada (3 aut., 5 aut., 10 aut.); Département de Pharmacologie, Faculté de Médecine, Université de Montréal/Montréal, QC, H3C 3J7/Canada (4 aut., 9 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Neuroscience; ISSN 0306-4522; Coden NRSCDN; Pays-Bas; Da. 2010; Vol. 169; No. 2; Pp. 932-949; Bibl. 1 p.</SO>
<LA>Anglais</LA>
<EA>DCC (deleted in colorectal cancer), a receptor for the axon guidance cue netrin-1, is highly expressed by mesencephalic dopaminergic (DA) neurons during development; however, the contribution of DCC to DA development remains largely uncharacterized. DA neurons in ventral mesencephalic nuclei also express UNC5 homologue netrin receptors from late embryogenesis to adulthood, raising the possibility that DA axons could be attracted or repelled by netrins. Examining newborn dcc null mice, we report that loss of DCC function results in profound alterations of DA circuitry, including DA progenitor cell migration defects, reduced numbers of DA cells in midbrain nuclei, an anomalous DA ventral commissure, malformed DA innervation of the ventral striatum, and reduced DA innervation of the cerebral cortex. Caspase-3 activation was detected in inappropriately localized DA cells, consistent with apoptosis contributing to reduced cell numbers. Dcc heterozygous mice express reduced levels of DCC protein. Although less severely disrupted than dcc nulls, newborn and adult dcc heterozygotes also have fewer DA neurons in ventral mesenscephalic nuclei. Despite the reduced numbers of DA neurons, newborn dcc heterozygotes and nulls exhibit similar DA innervation density as wild-type littermates in the nucleus accumbens core, and adult dcc heterozygotes exhibit increased DA innervation in medial prefrontal cortex. A trend towards increased innervation of medial prefrontal cortex was detected in newborn dcc heterozygotes, but did not reach statistical significance, suggesting that the increase in adult heterozygotes results from enhanced DA arborization during postnatal development. Consistent with the hypothesis that DCC regulates DA axonal projections, disrupting DCC function in culture inhibits netrin-1 induced DA axon extension and axon branching. Furthermore, disrupting DCC function in isolated DA neurons grown as micro-island cultures reduces the number of autaptic synapses per cell. We conclude that DCC regulates appropriate precursor cell migration, axon guidance, and terminal arborization by DA neurons.</EA>
<CC>002A25; 002B17G</CC>
<FD>Récepteur biologique; Dopamine; Axone; Synaptogenèse; Maladie de Parkinson; Schizophrénie</FD>
<FG>Catécholamine; Neurotransmetteur; Maladie dégénérative; Pathologie du système nerveux; Pathologie de l'encéphale; Syndrome extrapyramidal; Pathologie du système nerveux central; Psychose</FG>
<ED>Biological receptor; Dopamine; Axon; Synaptogenesis; Parkinson disease; Schizophrenia</ED>
<EG>Catecholamine; Neurotransmitter; Degenerative disease; Nervous system diseases; Cerebral disorder; Extrapyramidal syndrome; Central nervous system disease; Psychosis</EG>
<SD>Receptor biológico; Dopamina; Axón; Sinaptogénesis; Parkinson enfermedad; Esquizofrenia</SD>
<LO>INIST-17194.354000194123870350</LO>
<ID>10-0397347</ID>
</server>
</inist>
</record>
Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Canada/explor/ParkinsonCanadaV1/Data/PascalFrancis/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000405 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/PascalFrancis/Corpus/biblio.hfd -nk 000405 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien |wiki= Wicri/Canada |area= ParkinsonCanadaV1 |flux= PascalFrancis |étape= Corpus |type= RBID |clé= Pascal:10-0397347 |texte= CRITICAL ROLES FOR THE NETRIN RECEPTOR DELETED IN COLORECTAL CANCER IN DOPAMINERGIC NEURONAL PRECURSOR MIGRATION, AXON GUIDANCE, AND AXON ARBORIZATION }}
This area was generated with Dilib version V0.6.29. |