In Situ Hybridization of trkB and trkC Receptor mRNA in Rat Forebrain and Association with High-affinity Binding of [125I]BDNF, [125I]NT-4/5 and [125I]NT-3
The TrkB and TrkC receptor tyrosine kinases have been identified as high-affinity receptors for the neurotrophic factors brain-derived neurotrophic factor (BDNF) and neurotrophin-4/5 (NT-4/5) and NT-3 respectively. These receptor classes were identified and mapped by the in situ hybridization of ant...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Altar, C. Anthony [verfasserIn] Siuciak, Judith A. [verfasserIn] Wright, Paul [verfasserIn] |
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| Format: |
E-Artikel |
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| Erschienen: |
Oxford, UK: Blackwell Publishing Ltd ; 1994 |
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| Schlagwörter: |
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| Umfang: |
Online-Ressource |
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| Reproduktion: |
2006 ; Blackwell Publishing Journal Backfiles 1879-2005 |
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| Übergeordnetes Werk: |
In: European journal of neuroscience - Oxford [u.a.] : Blackwell, 1989, 6(1994), 9, Seite 0 |
| Übergeordnetes Werk: |
volume:6 ; year:1994 ; number:9 ; pages:0 |
| Links: |
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| DOI / URN: |
10.1111/j.1460-9568.1994.tb01001.x |
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| 245 | 1 | 0 | |a In Situ Hybridization of trkB and trkC Receptor mRNA in Rat Forebrain and Association with High-affinity Binding of [125I]BDNF, [125I]NT-4/5 and [125I]NT-3 |
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| 520 | |a The TrkB and TrkC receptor tyrosine kinases have been identified as high-affinity receptors for the neurotrophic factors brain-derived neurotrophic factor (BDNF) and neurotrophin-4/5 (NT-4/5) and NT-3 respectively. These receptor classes were identified and mapped by the in situ hybridization of antisense riboprobes complementary to portions of the intracellular (tyrosine kinase) or extracellular (ligand-binding) domains of trkB and trkC mRNA, and by the distribution of high-affinity [125I]BDNF, [125I]NT-4/5 and [125I]NT-3 binding sites in adjacent rat brain sections. Both methods showed that TrkB and TrkC receptors are abundant and widely expressed throughout the brain. Kinase or extracellular domain trkC probes labelled neuronal somata in a qualitatively similar manner in virtually every major area of the forebrain. Neither trkC probe labelled non-neuronal cells except for elements within cerebral arteries and arterioles. The kinase domain trkB probe hybridized exclusively to neurons. Neurons expressing trkB were even more widely distributed than those expressing trkC. The extracellular domain trkB probe labelled neurons with the same relative distribution as the trkB kinase domain probe, but also hybridized extensively with non-neural cells, particularly astrocytes, ependyma and choroid epithelium cells. The distribution of [125I]NT-3 binding sites generally resembled that of trkC hybridization, particularly in the neocortex, striatum and thalamus. [125I]BDNF and [125I]NT-4/5 binding sites were more widely distributed and denser than those for [125I]NT-3, and resembled the trkB hybridization pattern. These patterns are consistent with the preferential binding in the brain of TrkC receptors by [125I]NT-3 and of TrkB receptors by [125I]BDNF and [125I]NT-4/5. That the predominantly neuronal patterns of hybridization obtained with kinase and extracellular domain probes for trkC are qualitatively indistinguishable suggests that truncated and full-length forms of TrkC are expressed within extensively overlapping populations of neurons. In marked contrast to TrkC, expression of the full-length and truncated forms of TrkB appears to be largely segregated, being expressed principally on neurons and non-neuronal cells respectively. The abundant and widespread neuronal distribution of full-length, signal-transducing forms of TrkB and TrkC predict that their cognate ligands, BDNF, NT-4/5 and NT-3, may exert direct effects on a large proportion of neurons within the mature brain. | ||
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| 700 | 1 | |a Lindsay, Ronald M. |4 oth | |
| 700 | 1 | |a Wiegand, Stanley J. |4 oth | |
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10.1111/j.1460-9568.1994.tb01001.x doi (DE-627)NLEJ239885635 DE-627 ger DE-627 rakwb Altar, C. Anthony verfasserin aut In Situ Hybridization of trkB and trkC Receptor mRNA in Rat Forebrain and Association with High-affinity Binding of [125I]BDNF, [125I]NT-4/5 and [125I]NT-3 Oxford, UK Blackwell Publishing Ltd 1994 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The TrkB and TrkC receptor tyrosine kinases have been identified as high-affinity receptors for the neurotrophic factors brain-derived neurotrophic factor (BDNF) and neurotrophin-4/5 (NT-4/5) and NT-3 respectively. These receptor classes were identified and mapped by the in situ hybridization of antisense riboprobes complementary to portions of the intracellular (tyrosine kinase) or extracellular (ligand-binding) domains of trkB and trkC mRNA, and by the distribution of high-affinity [125I]BDNF, [125I]NT-4/5 and [125I]NT-3 binding sites in adjacent rat brain sections. Both methods showed that TrkB and TrkC receptors are abundant and widely expressed throughout the brain. Kinase or extracellular domain trkC probes labelled neuronal somata in a qualitatively similar manner in virtually every major area of the forebrain. Neither trkC probe labelled non-neuronal cells except for elements within cerebral arteries and arterioles. The kinase domain trkB probe hybridized exclusively to neurons. Neurons expressing trkB were even more widely distributed than those expressing trkC. The extracellular domain trkB probe labelled neurons with the same relative distribution as the trkB kinase domain probe, but also hybridized extensively with non-neural cells, particularly astrocytes, ependyma and choroid epithelium cells. The distribution of [125I]NT-3 binding sites generally resembled that of trkC hybridization, particularly in the neocortex, striatum and thalamus. [125I]BDNF and [125I]NT-4/5 binding sites were more widely distributed and denser than those for [125I]NT-3, and resembled the trkB hybridization pattern. These patterns are consistent with the preferential binding in the brain of TrkC receptors by [125I]NT-3 and of TrkB receptors by [125I]BDNF and [125I]NT-4/5. That the predominantly neuronal patterns of hybridization obtained with kinase and extracellular domain probes for trkC are qualitatively indistinguishable suggests that truncated and full-length forms of TrkC are expressed within extensively overlapping populations of neurons. In marked contrast to TrkC, expression of the full-length and truncated forms of TrkB appears to be largely segregated, being expressed principally on neurons and non-neuronal cells respectively. The abundant and widespread neuronal distribution of full-length, signal-transducing forms of TrkB and TrkC predict that their cognate ligands, BDNF, NT-4/5 and NT-3, may exert direct effects on a large proportion of neurons within the mature brain. 2006 Blackwell Publishing Journal Backfiles 1879-2005 |2006|||||||||| neurotrophic factor Siuciak, Judith A. verfasserin aut Wright, Paul verfasserin aut Ip, Nancy Y. oth Lindsay, Ronald M. oth Wiegand, Stanley J. oth In European journal of neuroscience Oxford [u.a.] : Blackwell, 1989 6(1994), 9, Seite 0 Online-Ressource (DE-627)NLEJ243926383 (DE-600)2005178-5 1460-9568 nnns volume:6 year:1994 number:9 pages:0 http://dx.doi.org/10.1111/j.1460-9568.1994.tb01001.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 6 1994 9 0 |
| spelling |
10.1111/j.1460-9568.1994.tb01001.x doi (DE-627)NLEJ239885635 DE-627 ger DE-627 rakwb Altar, C. Anthony verfasserin aut In Situ Hybridization of trkB and trkC Receptor mRNA in Rat Forebrain and Association with High-affinity Binding of [125I]BDNF, [125I]NT-4/5 and [125I]NT-3 Oxford, UK Blackwell Publishing Ltd 1994 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The TrkB and TrkC receptor tyrosine kinases have been identified as high-affinity receptors for the neurotrophic factors brain-derived neurotrophic factor (BDNF) and neurotrophin-4/5 (NT-4/5) and NT-3 respectively. These receptor classes were identified and mapped by the in situ hybridization of antisense riboprobes complementary to portions of the intracellular (tyrosine kinase) or extracellular (ligand-binding) domains of trkB and trkC mRNA, and by the distribution of high-affinity [125I]BDNF, [125I]NT-4/5 and [125I]NT-3 binding sites in adjacent rat brain sections. Both methods showed that TrkB and TrkC receptors are abundant and widely expressed throughout the brain. Kinase or extracellular domain trkC probes labelled neuronal somata in a qualitatively similar manner in virtually every major area of the forebrain. Neither trkC probe labelled non-neuronal cells except for elements within cerebral arteries and arterioles. The kinase domain trkB probe hybridized exclusively to neurons. Neurons expressing trkB were even more widely distributed than those expressing trkC. The extracellular domain trkB probe labelled neurons with the same relative distribution as the trkB kinase domain probe, but also hybridized extensively with non-neural cells, particularly astrocytes, ependyma and choroid epithelium cells. The distribution of [125I]NT-3 binding sites generally resembled that of trkC hybridization, particularly in the neocortex, striatum and thalamus. [125I]BDNF and [125I]NT-4/5 binding sites were more widely distributed and denser than those for [125I]NT-3, and resembled the trkB hybridization pattern. These patterns are consistent with the preferential binding in the brain of TrkC receptors by [125I]NT-3 and of TrkB receptors by [125I]BDNF and [125I]NT-4/5. That the predominantly neuronal patterns of hybridization obtained with kinase and extracellular domain probes for trkC are qualitatively indistinguishable suggests that truncated and full-length forms of TrkC are expressed within extensively overlapping populations of neurons. In marked contrast to TrkC, expression of the full-length and truncated forms of TrkB appears to be largely segregated, being expressed principally on neurons and non-neuronal cells respectively. The abundant and widespread neuronal distribution of full-length, signal-transducing forms of TrkB and TrkC predict that their cognate ligands, BDNF, NT-4/5 and NT-3, may exert direct effects on a large proportion of neurons within the mature brain. 2006 Blackwell Publishing Journal Backfiles 1879-2005 |2006|||||||||| neurotrophic factor Siuciak, Judith A. verfasserin aut Wright, Paul verfasserin aut Ip, Nancy Y. oth Lindsay, Ronald M. oth Wiegand, Stanley J. oth In European journal of neuroscience Oxford [u.a.] : Blackwell, 1989 6(1994), 9, Seite 0 Online-Ressource (DE-627)NLEJ243926383 (DE-600)2005178-5 1460-9568 nnns volume:6 year:1994 number:9 pages:0 http://dx.doi.org/10.1111/j.1460-9568.1994.tb01001.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 6 1994 9 0 |
| allfields_unstemmed |
10.1111/j.1460-9568.1994.tb01001.x doi (DE-627)NLEJ239885635 DE-627 ger DE-627 rakwb Altar, C. Anthony verfasserin aut In Situ Hybridization of trkB and trkC Receptor mRNA in Rat Forebrain and Association with High-affinity Binding of [125I]BDNF, [125I]NT-4/5 and [125I]NT-3 Oxford, UK Blackwell Publishing Ltd 1994 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The TrkB and TrkC receptor tyrosine kinases have been identified as high-affinity receptors for the neurotrophic factors brain-derived neurotrophic factor (BDNF) and neurotrophin-4/5 (NT-4/5) and NT-3 respectively. These receptor classes were identified and mapped by the in situ hybridization of antisense riboprobes complementary to portions of the intracellular (tyrosine kinase) or extracellular (ligand-binding) domains of trkB and trkC mRNA, and by the distribution of high-affinity [125I]BDNF, [125I]NT-4/5 and [125I]NT-3 binding sites in adjacent rat brain sections. Both methods showed that TrkB and TrkC receptors are abundant and widely expressed throughout the brain. Kinase or extracellular domain trkC probes labelled neuronal somata in a qualitatively similar manner in virtually every major area of the forebrain. Neither trkC probe labelled non-neuronal cells except for elements within cerebral arteries and arterioles. The kinase domain trkB probe hybridized exclusively to neurons. Neurons expressing trkB were even more widely distributed than those expressing trkC. The extracellular domain trkB probe labelled neurons with the same relative distribution as the trkB kinase domain probe, but also hybridized extensively with non-neural cells, particularly astrocytes, ependyma and choroid epithelium cells. The distribution of [125I]NT-3 binding sites generally resembled that of trkC hybridization, particularly in the neocortex, striatum and thalamus. [125I]BDNF and [125I]NT-4/5 binding sites were more widely distributed and denser than those for [125I]NT-3, and resembled the trkB hybridization pattern. These patterns are consistent with the preferential binding in the brain of TrkC receptors by [125I]NT-3 and of TrkB receptors by [125I]BDNF and [125I]NT-4/5. That the predominantly neuronal patterns of hybridization obtained with kinase and extracellular domain probes for trkC are qualitatively indistinguishable suggests that truncated and full-length forms of TrkC are expressed within extensively overlapping populations of neurons. In marked contrast to TrkC, expression of the full-length and truncated forms of TrkB appears to be largely segregated, being expressed principally on neurons and non-neuronal cells respectively. The abundant and widespread neuronal distribution of full-length, signal-transducing forms of TrkB and TrkC predict that their cognate ligands, BDNF, NT-4/5 and NT-3, may exert direct effects on a large proportion of neurons within the mature brain. 2006 Blackwell Publishing Journal Backfiles 1879-2005 |2006|||||||||| neurotrophic factor Siuciak, Judith A. verfasserin aut Wright, Paul verfasserin aut Ip, Nancy Y. oth Lindsay, Ronald M. oth Wiegand, Stanley J. oth In European journal of neuroscience Oxford [u.a.] : Blackwell, 1989 6(1994), 9, Seite 0 Online-Ressource (DE-627)NLEJ243926383 (DE-600)2005178-5 1460-9568 nnns volume:6 year:1994 number:9 pages:0 http://dx.doi.org/10.1111/j.1460-9568.1994.tb01001.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 6 1994 9 0 |
| allfieldsGer |
10.1111/j.1460-9568.1994.tb01001.x doi (DE-627)NLEJ239885635 DE-627 ger DE-627 rakwb Altar, C. Anthony verfasserin aut In Situ Hybridization of trkB and trkC Receptor mRNA in Rat Forebrain and Association with High-affinity Binding of [125I]BDNF, [125I]NT-4/5 and [125I]NT-3 Oxford, UK Blackwell Publishing Ltd 1994 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The TrkB and TrkC receptor tyrosine kinases have been identified as high-affinity receptors for the neurotrophic factors brain-derived neurotrophic factor (BDNF) and neurotrophin-4/5 (NT-4/5) and NT-3 respectively. These receptor classes were identified and mapped by the in situ hybridization of antisense riboprobes complementary to portions of the intracellular (tyrosine kinase) or extracellular (ligand-binding) domains of trkB and trkC mRNA, and by the distribution of high-affinity [125I]BDNF, [125I]NT-4/5 and [125I]NT-3 binding sites in adjacent rat brain sections. Both methods showed that TrkB and TrkC receptors are abundant and widely expressed throughout the brain. Kinase or extracellular domain trkC probes labelled neuronal somata in a qualitatively similar manner in virtually every major area of the forebrain. Neither trkC probe labelled non-neuronal cells except for elements within cerebral arteries and arterioles. The kinase domain trkB probe hybridized exclusively to neurons. Neurons expressing trkB were even more widely distributed than those expressing trkC. The extracellular domain trkB probe labelled neurons with the same relative distribution as the trkB kinase domain probe, but also hybridized extensively with non-neural cells, particularly astrocytes, ependyma and choroid epithelium cells. The distribution of [125I]NT-3 binding sites generally resembled that of trkC hybridization, particularly in the neocortex, striatum and thalamus. [125I]BDNF and [125I]NT-4/5 binding sites were more widely distributed and denser than those for [125I]NT-3, and resembled the trkB hybridization pattern. These patterns are consistent with the preferential binding in the brain of TrkC receptors by [125I]NT-3 and of TrkB receptors by [125I]BDNF and [125I]NT-4/5. That the predominantly neuronal patterns of hybridization obtained with kinase and extracellular domain probes for trkC are qualitatively indistinguishable suggests that truncated and full-length forms of TrkC are expressed within extensively overlapping populations of neurons. In marked contrast to TrkC, expression of the full-length and truncated forms of TrkB appears to be largely segregated, being expressed principally on neurons and non-neuronal cells respectively. The abundant and widespread neuronal distribution of full-length, signal-transducing forms of TrkB and TrkC predict that their cognate ligands, BDNF, NT-4/5 and NT-3, may exert direct effects on a large proportion of neurons within the mature brain. 2006 Blackwell Publishing Journal Backfiles 1879-2005 |2006|||||||||| neurotrophic factor Siuciak, Judith A. verfasserin aut Wright, Paul verfasserin aut Ip, Nancy Y. oth Lindsay, Ronald M. oth Wiegand, Stanley J. oth In European journal of neuroscience Oxford [u.a.] : Blackwell, 1989 6(1994), 9, Seite 0 Online-Ressource (DE-627)NLEJ243926383 (DE-600)2005178-5 1460-9568 nnns volume:6 year:1994 number:9 pages:0 http://dx.doi.org/10.1111/j.1460-9568.1994.tb01001.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 6 1994 9 0 |
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10.1111/j.1460-9568.1994.tb01001.x doi (DE-627)NLEJ239885635 DE-627 ger DE-627 rakwb Altar, C. Anthony verfasserin aut In Situ Hybridization of trkB and trkC Receptor mRNA in Rat Forebrain and Association with High-affinity Binding of [125I]BDNF, [125I]NT-4/5 and [125I]NT-3 Oxford, UK Blackwell Publishing Ltd 1994 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The TrkB and TrkC receptor tyrosine kinases have been identified as high-affinity receptors for the neurotrophic factors brain-derived neurotrophic factor (BDNF) and neurotrophin-4/5 (NT-4/5) and NT-3 respectively. These receptor classes were identified and mapped by the in situ hybridization of antisense riboprobes complementary to portions of the intracellular (tyrosine kinase) or extracellular (ligand-binding) domains of trkB and trkC mRNA, and by the distribution of high-affinity [125I]BDNF, [125I]NT-4/5 and [125I]NT-3 binding sites in adjacent rat brain sections. Both methods showed that TrkB and TrkC receptors are abundant and widely expressed throughout the brain. Kinase or extracellular domain trkC probes labelled neuronal somata in a qualitatively similar manner in virtually every major area of the forebrain. Neither trkC probe labelled non-neuronal cells except for elements within cerebral arteries and arterioles. The kinase domain trkB probe hybridized exclusively to neurons. Neurons expressing trkB were even more widely distributed than those expressing trkC. The extracellular domain trkB probe labelled neurons with the same relative distribution as the trkB kinase domain probe, but also hybridized extensively with non-neural cells, particularly astrocytes, ependyma and choroid epithelium cells. The distribution of [125I]NT-3 binding sites generally resembled that of trkC hybridization, particularly in the neocortex, striatum and thalamus. [125I]BDNF and [125I]NT-4/5 binding sites were more widely distributed and denser than those for [125I]NT-3, and resembled the trkB hybridization pattern. These patterns are consistent with the preferential binding in the brain of TrkC receptors by [125I]NT-3 and of TrkB receptors by [125I]BDNF and [125I]NT-4/5. That the predominantly neuronal patterns of hybridization obtained with kinase and extracellular domain probes for trkC are qualitatively indistinguishable suggests that truncated and full-length forms of TrkC are expressed within extensively overlapping populations of neurons. In marked contrast to TrkC, expression of the full-length and truncated forms of TrkB appears to be largely segregated, being expressed principally on neurons and non-neuronal cells respectively. The abundant and widespread neuronal distribution of full-length, signal-transducing forms of TrkB and TrkC predict that their cognate ligands, BDNF, NT-4/5 and NT-3, may exert direct effects on a large proportion of neurons within the mature brain. 2006 Blackwell Publishing Journal Backfiles 1879-2005 |2006|||||||||| neurotrophic factor Siuciak, Judith A. verfasserin aut Wright, Paul verfasserin aut Ip, Nancy Y. oth Lindsay, Ronald M. oth Wiegand, Stanley J. oth In European journal of neuroscience Oxford [u.a.] : Blackwell, 1989 6(1994), 9, Seite 0 Online-Ressource (DE-627)NLEJ243926383 (DE-600)2005178-5 1460-9568 nnns volume:6 year:1994 number:9 pages:0 http://dx.doi.org/10.1111/j.1460-9568.1994.tb01001.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 6 1994 9 0 |
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Anthony</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">In Situ Hybridization of trkB and trkC Receptor mRNA in Rat Forebrain and Association with High-affinity Binding of [125I]BDNF, [125I]NT-4/5 and [125I]NT-3</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="a">Oxford, UK</subfield><subfield code="b">Blackwell Publishing Ltd</subfield><subfield code="c">1994</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">The TrkB and TrkC receptor tyrosine kinases have been identified as high-affinity receptors for the neurotrophic factors brain-derived neurotrophic factor (BDNF) and neurotrophin-4/5 (NT-4/5) and NT-3 respectively. These receptor classes were identified and mapped by the in situ hybridization of antisense riboprobes complementary to portions of the intracellular (tyrosine kinase) or extracellular (ligand-binding) domains of trkB and trkC mRNA, and by the distribution of high-affinity [125I]BDNF, [125I]NT-4/5 and [125I]NT-3 binding sites in adjacent rat brain sections. Both methods showed that TrkB and TrkC receptors are abundant and widely expressed throughout the brain. Kinase or extracellular domain trkC probes labelled neuronal somata in a qualitatively similar manner in virtually every major area of the forebrain. Neither trkC probe labelled non-neuronal cells except for elements within cerebral arteries and arterioles. The kinase domain trkB probe hybridized exclusively to neurons. Neurons expressing trkB were even more widely distributed than those expressing trkC. The extracellular domain trkB probe labelled neurons with the same relative distribution as the trkB kinase domain probe, but also hybridized extensively with non-neural cells, particularly astrocytes, ependyma and choroid epithelium cells. The distribution of [125I]NT-3 binding sites generally resembled that of trkC hybridization, particularly in the neocortex, striatum and thalamus. [125I]BDNF and [125I]NT-4/5 binding sites were more widely distributed and denser than those for [125I]NT-3, and resembled the trkB hybridization pattern. These patterns are consistent with the preferential binding in the brain of TrkC receptors by [125I]NT-3 and of TrkB receptors by [125I]BDNF and [125I]NT-4/5. That the predominantly neuronal patterns of hybridization obtained with kinase and extracellular domain probes for trkC are qualitatively indistinguishable suggests that truncated and full-length forms of TrkC are expressed within extensively overlapping populations of neurons. In marked contrast to TrkC, expression of the full-length and truncated forms of TrkB appears to be largely segregated, being expressed principally on neurons and non-neuronal cells respectively. 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Blackwell Publishing Journal Backfiles 1879-2005 |
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Altar, C. Anthony |
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Altar, C. Anthony misc neurotrophic factor In Situ Hybridization of trkB and trkC Receptor mRNA in Rat Forebrain and Association with High-affinity Binding of [125I]BDNF, [125I]NT-4/5 and [125I]NT-3 |
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In Situ Hybridization of trkB and trkC Receptor mRNA in Rat Forebrain and Association with High-affinity Binding of [125I]BDNF, [125I]NT-4/5 and [125I]NT-3 neurotrophic factor |
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In Situ Hybridization of trkB and trkC Receptor mRNA in Rat Forebrain and Association with High-affinity Binding of [125I]BDNF, [125I]NT-4/5 and [125I]NT-3 |
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In Situ Hybridization of trkB and trkC Receptor mRNA in Rat Forebrain and Association with High-affinity Binding of [125I]BDNF, [125I]NT-4/5 and [125I]NT-3 |
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in situ hybridization of trkb and trkc receptor mrna in rat forebrain and association with high-affinity binding of [125i]bdnf, [125i]nt-4/5 and [125i]nt-3 |
| title_auth |
In Situ Hybridization of trkB and trkC Receptor mRNA in Rat Forebrain and Association with High-affinity Binding of [125I]BDNF, [125I]NT-4/5 and [125I]NT-3 |
| abstract |
The TrkB and TrkC receptor tyrosine kinases have been identified as high-affinity receptors for the neurotrophic factors brain-derived neurotrophic factor (BDNF) and neurotrophin-4/5 (NT-4/5) and NT-3 respectively. These receptor classes were identified and mapped by the in situ hybridization of antisense riboprobes complementary to portions of the intracellular (tyrosine kinase) or extracellular (ligand-binding) domains of trkB and trkC mRNA, and by the distribution of high-affinity [125I]BDNF, [125I]NT-4/5 and [125I]NT-3 binding sites in adjacent rat brain sections. Both methods showed that TrkB and TrkC receptors are abundant and widely expressed throughout the brain. Kinase or extracellular domain trkC probes labelled neuronal somata in a qualitatively similar manner in virtually every major area of the forebrain. Neither trkC probe labelled non-neuronal cells except for elements within cerebral arteries and arterioles. The kinase domain trkB probe hybridized exclusively to neurons. Neurons expressing trkB were even more widely distributed than those expressing trkC. The extracellular domain trkB probe labelled neurons with the same relative distribution as the trkB kinase domain probe, but also hybridized extensively with non-neural cells, particularly astrocytes, ependyma and choroid epithelium cells. The distribution of [125I]NT-3 binding sites generally resembled that of trkC hybridization, particularly in the neocortex, striatum and thalamus. [125I]BDNF and [125I]NT-4/5 binding sites were more widely distributed and denser than those for [125I]NT-3, and resembled the trkB hybridization pattern. These patterns are consistent with the preferential binding in the brain of TrkC receptors by [125I]NT-3 and of TrkB receptors by [125I]BDNF and [125I]NT-4/5. That the predominantly neuronal patterns of hybridization obtained with kinase and extracellular domain probes for trkC are qualitatively indistinguishable suggests that truncated and full-length forms of TrkC are expressed within extensively overlapping populations of neurons. In marked contrast to TrkC, expression of the full-length and truncated forms of TrkB appears to be largely segregated, being expressed principally on neurons and non-neuronal cells respectively. The abundant and widespread neuronal distribution of full-length, signal-transducing forms of TrkB and TrkC predict that their cognate ligands, BDNF, NT-4/5 and NT-3, may exert direct effects on a large proportion of neurons within the mature brain. |
| abstractGer |
The TrkB and TrkC receptor tyrosine kinases have been identified as high-affinity receptors for the neurotrophic factors brain-derived neurotrophic factor (BDNF) and neurotrophin-4/5 (NT-4/5) and NT-3 respectively. These receptor classes were identified and mapped by the in situ hybridization of antisense riboprobes complementary to portions of the intracellular (tyrosine kinase) or extracellular (ligand-binding) domains of trkB and trkC mRNA, and by the distribution of high-affinity [125I]BDNF, [125I]NT-4/5 and [125I]NT-3 binding sites in adjacent rat brain sections. Both methods showed that TrkB and TrkC receptors are abundant and widely expressed throughout the brain. Kinase or extracellular domain trkC probes labelled neuronal somata in a qualitatively similar manner in virtually every major area of the forebrain. Neither trkC probe labelled non-neuronal cells except for elements within cerebral arteries and arterioles. The kinase domain trkB probe hybridized exclusively to neurons. Neurons expressing trkB were even more widely distributed than those expressing trkC. The extracellular domain trkB probe labelled neurons with the same relative distribution as the trkB kinase domain probe, but also hybridized extensively with non-neural cells, particularly astrocytes, ependyma and choroid epithelium cells. The distribution of [125I]NT-3 binding sites generally resembled that of trkC hybridization, particularly in the neocortex, striatum and thalamus. [125I]BDNF and [125I]NT-4/5 binding sites were more widely distributed and denser than those for [125I]NT-3, and resembled the trkB hybridization pattern. These patterns are consistent with the preferential binding in the brain of TrkC receptors by [125I]NT-3 and of TrkB receptors by [125I]BDNF and [125I]NT-4/5. That the predominantly neuronal patterns of hybridization obtained with kinase and extracellular domain probes for trkC are qualitatively indistinguishable suggests that truncated and full-length forms of TrkC are expressed within extensively overlapping populations of neurons. In marked contrast to TrkC, expression of the full-length and truncated forms of TrkB appears to be largely segregated, being expressed principally on neurons and non-neuronal cells respectively. The abundant and widespread neuronal distribution of full-length, signal-transducing forms of TrkB and TrkC predict that their cognate ligands, BDNF, NT-4/5 and NT-3, may exert direct effects on a large proportion of neurons within the mature brain. |
| abstract_unstemmed |
The TrkB and TrkC receptor tyrosine kinases have been identified as high-affinity receptors for the neurotrophic factors brain-derived neurotrophic factor (BDNF) and neurotrophin-4/5 (NT-4/5) and NT-3 respectively. These receptor classes were identified and mapped by the in situ hybridization of antisense riboprobes complementary to portions of the intracellular (tyrosine kinase) or extracellular (ligand-binding) domains of trkB and trkC mRNA, and by the distribution of high-affinity [125I]BDNF, [125I]NT-4/5 and [125I]NT-3 binding sites in adjacent rat brain sections. Both methods showed that TrkB and TrkC receptors are abundant and widely expressed throughout the brain. Kinase or extracellular domain trkC probes labelled neuronal somata in a qualitatively similar manner in virtually every major area of the forebrain. Neither trkC probe labelled non-neuronal cells except for elements within cerebral arteries and arterioles. The kinase domain trkB probe hybridized exclusively to neurons. Neurons expressing trkB were even more widely distributed than those expressing trkC. The extracellular domain trkB probe labelled neurons with the same relative distribution as the trkB kinase domain probe, but also hybridized extensively with non-neural cells, particularly astrocytes, ependyma and choroid epithelium cells. The distribution of [125I]NT-3 binding sites generally resembled that of trkC hybridization, particularly in the neocortex, striatum and thalamus. [125I]BDNF and [125I]NT-4/5 binding sites were more widely distributed and denser than those for [125I]NT-3, and resembled the trkB hybridization pattern. These patterns are consistent with the preferential binding in the brain of TrkC receptors by [125I]NT-3 and of TrkB receptors by [125I]BDNF and [125I]NT-4/5. That the predominantly neuronal patterns of hybridization obtained with kinase and extracellular domain probes for trkC are qualitatively indistinguishable suggests that truncated and full-length forms of TrkC are expressed within extensively overlapping populations of neurons. In marked contrast to TrkC, expression of the full-length and truncated forms of TrkB appears to be largely segregated, being expressed principally on neurons and non-neuronal cells respectively. The abundant and widespread neuronal distribution of full-length, signal-transducing forms of TrkB and TrkC predict that their cognate ligands, BDNF, NT-4/5 and NT-3, may exert direct effects on a large proportion of neurons within the mature brain. |
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In Situ Hybridization of trkB and trkC Receptor mRNA in Rat Forebrain and Association with High-affinity Binding of [125I]BDNF, [125I]NT-4/5 and [125I]NT-3 |
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