Regional and subtype selective changes of neurotransmitter receptor density in a rat transgenic for the Huntington's disease mutation
Huntington's disease (HD) is an autosomal dominantly inherited progressive neurodegenerative disorder caused by a CAG/polyglutamine repeat expansion in the gene encoding the huntingtin protein. We have recently generated a rat model transgenic for HD, which displays a slowly progressive phenoty...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Bauer, Andreas [verfasserIn] Zilles, Karl [verfasserIn] Matusch, Andreas [verfasserIn] |
|---|
| Format: |
E-Artikel |
|---|
| Erschienen: |
Oxford, UK: Blackwell Science Ltd ; 2005 |
|---|
| Schlagwörter: |
|---|
| Umfang: |
Online-Ressource |
|---|
| Reproduktion: |
2005 ; Blackwell Publishing Journal Backfiles 1879-2005 |
|---|---|
| Übergeordnetes Werk: |
In: Journal of neurochemistry - Oxford : Wiley-Blackwell, 1956, 94(2005), 3, Seite 0 |
| Übergeordnetes Werk: |
volume:94 ; year:2005 ; number:3 ; pages:0 |
| Links: |
|---|
| DOI / URN: |
10.1111/j.1471-4159.2005.03169.x |
|---|
| Katalog-ID: |
NLEJ243113722 |
|---|
| LEADER | 01000caa a22002652 4500 | ||
|---|---|---|---|
| 001 | NLEJ243113722 | ||
| 003 | DE-627 | ||
| 005 | 20230506005826.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 120427s2005 xx |||||o 00| ||und c | ||
| 024 | 7 | |a 10.1111/j.1471-4159.2005.03169.x |2 doi | |
| 035 | |a (DE-627)NLEJ243113722 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 100 | 1 | |a Bauer, Andreas |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Regional and subtype selective changes of neurotransmitter receptor density in a rat transgenic for the Huntington's disease mutation |
| 264 | 1 | |a Oxford, UK |b Blackwell Science Ltd |c 2005 | |
| 300 | |a Online-Ressource | ||
| 336 | |a nicht spezifiziert |b zzz |2 rdacontent | ||
| 337 | |a nicht spezifiziert |b z |2 rdamedia | ||
| 338 | |a nicht spezifiziert |b zu |2 rdacarrier | ||
| 520 | |a Huntington's disease (HD) is an autosomal dominantly inherited progressive neurodegenerative disorder caused by a CAG/polyglutamine repeat expansion in the gene encoding the huntingtin protein. We have recently generated a rat model transgenic for HD, which displays a slowly progressive phenotype resembling the human adult-onset type of disease. In this study we systematically assessed the distribution and density of 17 transmitter receptors in the brains of 2-year-old rats using quantitative multi-tracer autoradiography and high-resolution positron emission tomography. Heterozygous animals expressed increased densities of M2 acetylcholine (increase of 148 ± 16% of controls; p > 0.001; n = 7), nicotine (increase of 149 ± 16% of controls; p > 0.01; n = 6), and α2 noradrenergic receptors (increase of 141 ± 15% of controls; p > 0.001; n = 6), respectively. Densities of these receptors were decreased in homozygous animals. Decreases of receptor density in both hetero- and homozygous animals were found for M1 acetylcholine, 5-HT2A serotonin, A2A adenosine, D1 and D2 dopamine, and GABAA receptors, respectively. Other investigated receptor systems showed small changes or were not affected. The present data suggest that the moderate increase of CAG/polyglutamine repeat expansions in the present rat model of Huntington's disease is characterized by subtype-selective and region-specific changes of neuroreceptor densities. In particular, there is evidence for a contribution of predominantly presynaptically localized cholinergic and noradrenergic receptors in the response to Huntington's disease pathology. | ||
| 533 | |d 2005 |f Blackwell Publishing Journal Backfiles 1879-2005 |7 |2005|||||||||| | ||
| 650 | 4 | |a Huntington's disease | |
| 700 | 1 | |a Zilles, Karl |e verfasserin |4 aut | |
| 700 | 1 | |a Matusch, Andreas |e verfasserin |4 aut | |
| 700 | 1 | |a Holzmann, Carsten |4 oth | |
| 700 | 1 | |a Riess, Olaf |4 oth | |
| 700 | 1 | |a Von Hörsten, Stephan |4 oth | |
| 773 | 0 | 8 | |i In |t Journal of neurochemistry |d Oxford : Wiley-Blackwell, 1956 |g 94(2005), 3, Seite 0 |h Online-Ressource |w (DE-627)NLEJ243927584 |w (DE-600)2020528-4 |x 1471-4159 |7 nnns |
| 773 | 1 | 8 | |g volume:94 |g year:2005 |g number:3 |g pages:0 |
| 856 | 4 | 0 | |u http://dx.doi.org/10.1111/j.1471-4159.2005.03169.x |q text/html |x Verlag |z Deutschlandweit zugänglich |3 Volltext |
| 912 | |a GBV_USEFLAG_U | ||
| 912 | |a ZDB-1-DJB | ||
| 912 | |a GBV_NL_ARTICLE | ||
| 951 | |a AR | ||
| 952 | |d 94 |j 2005 |e 3 |h 0 | ||
| author_variant |
a b ab k z kz a m am |
|---|---|
| matchkey_str |
article:14714159:2005----::einlnsbyeeetvcagsfertasitreetrestiaataseif |
| hierarchy_sort_str |
2005 |
| publishDate |
2005 |
| allfields |
10.1111/j.1471-4159.2005.03169.x doi (DE-627)NLEJ243113722 DE-627 ger DE-627 rakwb Bauer, Andreas verfasserin aut Regional and subtype selective changes of neurotransmitter receptor density in a rat transgenic for the Huntington's disease mutation Oxford, UK Blackwell Science Ltd 2005 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Huntington's disease (HD) is an autosomal dominantly inherited progressive neurodegenerative disorder caused by a CAG/polyglutamine repeat expansion in the gene encoding the huntingtin protein. We have recently generated a rat model transgenic for HD, which displays a slowly progressive phenotype resembling the human adult-onset type of disease. In this study we systematically assessed the distribution and density of 17 transmitter receptors in the brains of 2-year-old rats using quantitative multi-tracer autoradiography and high-resolution positron emission tomography. Heterozygous animals expressed increased densities of M2 acetylcholine (increase of 148 ± 16% of controls; p > 0.001; n = 7), nicotine (increase of 149 ± 16% of controls; p > 0.01; n = 6), and α2 noradrenergic receptors (increase of 141 ± 15% of controls; p > 0.001; n = 6), respectively. Densities of these receptors were decreased in homozygous animals. Decreases of receptor density in both hetero- and homozygous animals were found for M1 acetylcholine, 5-HT2A serotonin, A2A adenosine, D1 and D2 dopamine, and GABAA receptors, respectively. Other investigated receptor systems showed small changes or were not affected. The present data suggest that the moderate increase of CAG/polyglutamine repeat expansions in the present rat model of Huntington's disease is characterized by subtype-selective and region-specific changes of neuroreceptor densities. In particular, there is evidence for a contribution of predominantly presynaptically localized cholinergic and noradrenergic receptors in the response to Huntington's disease pathology. 2005 Blackwell Publishing Journal Backfiles 1879-2005 |2005|||||||||| Huntington's disease Zilles, Karl verfasserin aut Matusch, Andreas verfasserin aut Holzmann, Carsten oth Riess, Olaf oth Von Hörsten, Stephan oth In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 94(2005), 3, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:94 year:2005 number:3 pages:0 http://dx.doi.org/10.1111/j.1471-4159.2005.03169.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 94 2005 3 0 |
| spelling |
10.1111/j.1471-4159.2005.03169.x doi (DE-627)NLEJ243113722 DE-627 ger DE-627 rakwb Bauer, Andreas verfasserin aut Regional and subtype selective changes of neurotransmitter receptor density in a rat transgenic for the Huntington's disease mutation Oxford, UK Blackwell Science Ltd 2005 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Huntington's disease (HD) is an autosomal dominantly inherited progressive neurodegenerative disorder caused by a CAG/polyglutamine repeat expansion in the gene encoding the huntingtin protein. We have recently generated a rat model transgenic for HD, which displays a slowly progressive phenotype resembling the human adult-onset type of disease. In this study we systematically assessed the distribution and density of 17 transmitter receptors in the brains of 2-year-old rats using quantitative multi-tracer autoradiography and high-resolution positron emission tomography. Heterozygous animals expressed increased densities of M2 acetylcholine (increase of 148 ± 16% of controls; p > 0.001; n = 7), nicotine (increase of 149 ± 16% of controls; p > 0.01; n = 6), and α2 noradrenergic receptors (increase of 141 ± 15% of controls; p > 0.001; n = 6), respectively. Densities of these receptors were decreased in homozygous animals. Decreases of receptor density in both hetero- and homozygous animals were found for M1 acetylcholine, 5-HT2A serotonin, A2A adenosine, D1 and D2 dopamine, and GABAA receptors, respectively. Other investigated receptor systems showed small changes or were not affected. The present data suggest that the moderate increase of CAG/polyglutamine repeat expansions in the present rat model of Huntington's disease is characterized by subtype-selective and region-specific changes of neuroreceptor densities. In particular, there is evidence for a contribution of predominantly presynaptically localized cholinergic and noradrenergic receptors in the response to Huntington's disease pathology. 2005 Blackwell Publishing Journal Backfiles 1879-2005 |2005|||||||||| Huntington's disease Zilles, Karl verfasserin aut Matusch, Andreas verfasserin aut Holzmann, Carsten oth Riess, Olaf oth Von Hörsten, Stephan oth In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 94(2005), 3, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:94 year:2005 number:3 pages:0 http://dx.doi.org/10.1111/j.1471-4159.2005.03169.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 94 2005 3 0 |
| allfields_unstemmed |
10.1111/j.1471-4159.2005.03169.x doi (DE-627)NLEJ243113722 DE-627 ger DE-627 rakwb Bauer, Andreas verfasserin aut Regional and subtype selective changes of neurotransmitter receptor density in a rat transgenic for the Huntington's disease mutation Oxford, UK Blackwell Science Ltd 2005 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Huntington's disease (HD) is an autosomal dominantly inherited progressive neurodegenerative disorder caused by a CAG/polyglutamine repeat expansion in the gene encoding the huntingtin protein. We have recently generated a rat model transgenic for HD, which displays a slowly progressive phenotype resembling the human adult-onset type of disease. In this study we systematically assessed the distribution and density of 17 transmitter receptors in the brains of 2-year-old rats using quantitative multi-tracer autoradiography and high-resolution positron emission tomography. Heterozygous animals expressed increased densities of M2 acetylcholine (increase of 148 ± 16% of controls; p > 0.001; n = 7), nicotine (increase of 149 ± 16% of controls; p > 0.01; n = 6), and α2 noradrenergic receptors (increase of 141 ± 15% of controls; p > 0.001; n = 6), respectively. Densities of these receptors were decreased in homozygous animals. Decreases of receptor density in both hetero- and homozygous animals were found for M1 acetylcholine, 5-HT2A serotonin, A2A adenosine, D1 and D2 dopamine, and GABAA receptors, respectively. Other investigated receptor systems showed small changes or were not affected. The present data suggest that the moderate increase of CAG/polyglutamine repeat expansions in the present rat model of Huntington's disease is characterized by subtype-selective and region-specific changes of neuroreceptor densities. In particular, there is evidence for a contribution of predominantly presynaptically localized cholinergic and noradrenergic receptors in the response to Huntington's disease pathology. 2005 Blackwell Publishing Journal Backfiles 1879-2005 |2005|||||||||| Huntington's disease Zilles, Karl verfasserin aut Matusch, Andreas verfasserin aut Holzmann, Carsten oth Riess, Olaf oth Von Hörsten, Stephan oth In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 94(2005), 3, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:94 year:2005 number:3 pages:0 http://dx.doi.org/10.1111/j.1471-4159.2005.03169.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 94 2005 3 0 |
| allfieldsGer |
10.1111/j.1471-4159.2005.03169.x doi (DE-627)NLEJ243113722 DE-627 ger DE-627 rakwb Bauer, Andreas verfasserin aut Regional and subtype selective changes of neurotransmitter receptor density in a rat transgenic for the Huntington's disease mutation Oxford, UK Blackwell Science Ltd 2005 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Huntington's disease (HD) is an autosomal dominantly inherited progressive neurodegenerative disorder caused by a CAG/polyglutamine repeat expansion in the gene encoding the huntingtin protein. We have recently generated a rat model transgenic for HD, which displays a slowly progressive phenotype resembling the human adult-onset type of disease. In this study we systematically assessed the distribution and density of 17 transmitter receptors in the brains of 2-year-old rats using quantitative multi-tracer autoradiography and high-resolution positron emission tomography. Heterozygous animals expressed increased densities of M2 acetylcholine (increase of 148 ± 16% of controls; p > 0.001; n = 7), nicotine (increase of 149 ± 16% of controls; p > 0.01; n = 6), and α2 noradrenergic receptors (increase of 141 ± 15% of controls; p > 0.001; n = 6), respectively. Densities of these receptors were decreased in homozygous animals. Decreases of receptor density in both hetero- and homozygous animals were found for M1 acetylcholine, 5-HT2A serotonin, A2A adenosine, D1 and D2 dopamine, and GABAA receptors, respectively. Other investigated receptor systems showed small changes or were not affected. The present data suggest that the moderate increase of CAG/polyglutamine repeat expansions in the present rat model of Huntington's disease is characterized by subtype-selective and region-specific changes of neuroreceptor densities. In particular, there is evidence for a contribution of predominantly presynaptically localized cholinergic and noradrenergic receptors in the response to Huntington's disease pathology. 2005 Blackwell Publishing Journal Backfiles 1879-2005 |2005|||||||||| Huntington's disease Zilles, Karl verfasserin aut Matusch, Andreas verfasserin aut Holzmann, Carsten oth Riess, Olaf oth Von Hörsten, Stephan oth In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 94(2005), 3, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:94 year:2005 number:3 pages:0 http://dx.doi.org/10.1111/j.1471-4159.2005.03169.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 94 2005 3 0 |
| allfieldsSound |
10.1111/j.1471-4159.2005.03169.x doi (DE-627)NLEJ243113722 DE-627 ger DE-627 rakwb Bauer, Andreas verfasserin aut Regional and subtype selective changes of neurotransmitter receptor density in a rat transgenic for the Huntington's disease mutation Oxford, UK Blackwell Science Ltd 2005 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Huntington's disease (HD) is an autosomal dominantly inherited progressive neurodegenerative disorder caused by a CAG/polyglutamine repeat expansion in the gene encoding the huntingtin protein. We have recently generated a rat model transgenic for HD, which displays a slowly progressive phenotype resembling the human adult-onset type of disease. In this study we systematically assessed the distribution and density of 17 transmitter receptors in the brains of 2-year-old rats using quantitative multi-tracer autoradiography and high-resolution positron emission tomography. Heterozygous animals expressed increased densities of M2 acetylcholine (increase of 148 ± 16% of controls; p > 0.001; n = 7), nicotine (increase of 149 ± 16% of controls; p > 0.01; n = 6), and α2 noradrenergic receptors (increase of 141 ± 15% of controls; p > 0.001; n = 6), respectively. Densities of these receptors were decreased in homozygous animals. Decreases of receptor density in both hetero- and homozygous animals were found for M1 acetylcholine, 5-HT2A serotonin, A2A adenosine, D1 and D2 dopamine, and GABAA receptors, respectively. Other investigated receptor systems showed small changes or were not affected. The present data suggest that the moderate increase of CAG/polyglutamine repeat expansions in the present rat model of Huntington's disease is characterized by subtype-selective and region-specific changes of neuroreceptor densities. In particular, there is evidence for a contribution of predominantly presynaptically localized cholinergic and noradrenergic receptors in the response to Huntington's disease pathology. 2005 Blackwell Publishing Journal Backfiles 1879-2005 |2005|||||||||| Huntington's disease Zilles, Karl verfasserin aut Matusch, Andreas verfasserin aut Holzmann, Carsten oth Riess, Olaf oth Von Hörsten, Stephan oth In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 94(2005), 3, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:94 year:2005 number:3 pages:0 http://dx.doi.org/10.1111/j.1471-4159.2005.03169.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 94 2005 3 0 |
| source |
In Journal of neurochemistry 94(2005), 3, Seite 0 volume:94 year:2005 number:3 pages:0 |
| sourceStr |
In Journal of neurochemistry 94(2005), 3, Seite 0 volume:94 year:2005 number:3 pages:0 |
| format_phy_str_mv |
Article |
| institution |
findex.gbv.de |
| topic_facet |
Huntington's disease |
| isfreeaccess_bool |
false |
| container_title |
Journal of neurochemistry |
| authorswithroles_txt_mv |
Bauer, Andreas @@aut@@ Zilles, Karl @@aut@@ Matusch, Andreas @@aut@@ Holzmann, Carsten @@oth@@ Riess, Olaf @@oth@@ Von Hörsten, Stephan @@oth@@ |
| publishDateDaySort_date |
2005-01-01T00:00:00Z |
| hierarchy_top_id |
NLEJ243927584 |
| id |
NLEJ243113722 |
| fullrecord |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">NLEJ243113722</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230506005826.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">120427s2005 xx |||||o 00| ||und c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1111/j.1471-4159.2005.03169.x</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)NLEJ243113722</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Bauer, Andreas</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Regional and subtype selective changes of neurotransmitter receptor density in a rat transgenic for the Huntington's disease mutation</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="a">Oxford, UK</subfield><subfield code="b">Blackwell Science Ltd</subfield><subfield code="c">2005</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">Huntington's disease (HD) is an autosomal dominantly inherited progressive neurodegenerative disorder caused by a CAG/polyglutamine repeat expansion in the gene encoding the huntingtin protein. We have recently generated a rat model transgenic for HD, which displays a slowly progressive phenotype resembling the human adult-onset type of disease. In this study we systematically assessed the distribution and density of 17 transmitter receptors in the brains of 2-year-old rats using quantitative multi-tracer autoradiography and high-resolution positron emission tomography. Heterozygous animals expressed increased densities of M2 acetylcholine (increase of 148 ± 16% of controls; p > 0.001; n = 7), nicotine (increase of 149 ± 16% of controls; p > 0.01; n = 6), and α2 noradrenergic receptors (increase of 141 ± 15% of controls; p > 0.001; n = 6), respectively. Densities of these receptors were decreased in homozygous animals. Decreases of receptor density in both hetero- and homozygous animals were found for M1 acetylcholine, 5-HT2A serotonin, A2A adenosine, D1 and D2 dopamine, and GABAA receptors, respectively. Other investigated receptor systems showed small changes or were not affected. The present data suggest that the moderate increase of CAG/polyglutamine repeat expansions in the present rat model of Huntington's disease is characterized by subtype-selective and region-specific changes of neuroreceptor densities. In particular, there is evidence for a contribution of predominantly presynaptically localized cholinergic and noradrenergic receptors in the response to Huntington's disease pathology.</subfield></datafield><datafield tag="533" ind1=" " ind2=" "><subfield code="d">2005</subfield><subfield code="f">Blackwell Publishing Journal Backfiles 1879-2005</subfield><subfield code="7">|2005||||||||||</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Huntington's disease</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Zilles, Karl</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Matusch, Andreas</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Holzmann, Carsten</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Riess, Olaf</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Von Hörsten, Stephan</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">In</subfield><subfield code="t">Journal of neurochemistry</subfield><subfield code="d">Oxford : Wiley-Blackwell, 1956</subfield><subfield code="g">94(2005), 3, Seite 0</subfield><subfield code="h">Online-Ressource</subfield><subfield code="w">(DE-627)NLEJ243927584</subfield><subfield code="w">(DE-600)2020528-4</subfield><subfield code="x">1471-4159</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:94</subfield><subfield code="g">year:2005</subfield><subfield code="g">number:3</subfield><subfield code="g">pages:0</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">http://dx.doi.org/10.1111/j.1471-4159.2005.03169.x</subfield><subfield code="q">text/html</subfield><subfield code="x">Verlag</subfield><subfield code="z">Deutschlandweit zugänglich</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">ZDB-1-DJB</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_NL_ARTICLE</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">94</subfield><subfield code="j">2005</subfield><subfield code="e">3</subfield><subfield code="h">0</subfield></datafield></record></collection>
|
| series2 |
Blackwell Publishing Journal Backfiles 1879-2005 |
| author |
Bauer, Andreas |
| spellingShingle |
Bauer, Andreas misc Huntington's disease Regional and subtype selective changes of neurotransmitter receptor density in a rat transgenic for the Huntington's disease mutation |
| authorStr |
Bauer, Andreas |
| ppnlink_with_tag_str_mv |
@@773@@(DE-627)NLEJ243927584 |
| format |
electronic Article |
| delete_txt_mv |
keep |
| author_role |
aut aut aut |
| collection |
NL |
| publishPlace |
Oxford, UK |
| remote_str |
true |
| illustrated |
Not Illustrated |
| issn |
1471-4159 |
| topic_title |
Regional and subtype selective changes of neurotransmitter receptor density in a rat transgenic for the Huntington's disease mutation Huntington's disease |
| publisher |
Blackwell Science Ltd |
| publisherStr |
Blackwell Science Ltd |
| topic |
misc Huntington's disease |
| topic_unstemmed |
misc Huntington's disease |
| topic_browse |
misc Huntington's disease |
| format_facet |
Elektronische Aufsätze Aufsätze Elektronische Ressource |
| format_main_str_mv |
Text Zeitschrift/Artikel |
| carriertype_str_mv |
zu |
| author2_variant |
c h ch o r or h s v hs hsv |
| hierarchy_parent_title |
Journal of neurochemistry |
| hierarchy_parent_id |
NLEJ243927584 |
| hierarchy_top_title |
Journal of neurochemistry |
| isfreeaccess_txt |
false |
| familylinks_str_mv |
(DE-627)NLEJ243927584 (DE-600)2020528-4 |
| title |
Regional and subtype selective changes of neurotransmitter receptor density in a rat transgenic for the Huntington's disease mutation |
| ctrlnum |
(DE-627)NLEJ243113722 |
| title_full |
Regional and subtype selective changes of neurotransmitter receptor density in a rat transgenic for the Huntington's disease mutation |
| author_sort |
Bauer, Andreas |
| journal |
Journal of neurochemistry |
| journalStr |
Journal of neurochemistry |
| isOA_bool |
false |
| recordtype |
marc |
| publishDateSort |
2005 |
| contenttype_str_mv |
zzz |
| container_start_page |
0 |
| author_browse |
Bauer, Andreas Zilles, Karl Matusch, Andreas |
| container_volume |
94 |
| physical |
Online-Ressource |
| format_se |
Elektronische Aufsätze |
| author-letter |
Bauer, Andreas |
| doi_str_mv |
10.1111/j.1471-4159.2005.03169.x |
| author2-role |
verfasserin |
| title_sort |
regional and subtype selective changes of neurotransmitter receptor density in a rat transgenic for the huntington's disease mutation |
| title_auth |
Regional and subtype selective changes of neurotransmitter receptor density in a rat transgenic for the Huntington's disease mutation |
| abstract |
Huntington's disease (HD) is an autosomal dominantly inherited progressive neurodegenerative disorder caused by a CAG/polyglutamine repeat expansion in the gene encoding the huntingtin protein. We have recently generated a rat model transgenic for HD, which displays a slowly progressive phenotype resembling the human adult-onset type of disease. In this study we systematically assessed the distribution and density of 17 transmitter receptors in the brains of 2-year-old rats using quantitative multi-tracer autoradiography and high-resolution positron emission tomography. Heterozygous animals expressed increased densities of M2 acetylcholine (increase of 148 ± 16% of controls; p > 0.001; n = 7), nicotine (increase of 149 ± 16% of controls; p > 0.01; n = 6), and α2 noradrenergic receptors (increase of 141 ± 15% of controls; p > 0.001; n = 6), respectively. Densities of these receptors were decreased in homozygous animals. Decreases of receptor density in both hetero- and homozygous animals were found for M1 acetylcholine, 5-HT2A serotonin, A2A adenosine, D1 and D2 dopamine, and GABAA receptors, respectively. Other investigated receptor systems showed small changes or were not affected. The present data suggest that the moderate increase of CAG/polyglutamine repeat expansions in the present rat model of Huntington's disease is characterized by subtype-selective and region-specific changes of neuroreceptor densities. In particular, there is evidence for a contribution of predominantly presynaptically localized cholinergic and noradrenergic receptors in the response to Huntington's disease pathology. |
| abstractGer |
Huntington's disease (HD) is an autosomal dominantly inherited progressive neurodegenerative disorder caused by a CAG/polyglutamine repeat expansion in the gene encoding the huntingtin protein. We have recently generated a rat model transgenic for HD, which displays a slowly progressive phenotype resembling the human adult-onset type of disease. In this study we systematically assessed the distribution and density of 17 transmitter receptors in the brains of 2-year-old rats using quantitative multi-tracer autoradiography and high-resolution positron emission tomography. Heterozygous animals expressed increased densities of M2 acetylcholine (increase of 148 ± 16% of controls; p > 0.001; n = 7), nicotine (increase of 149 ± 16% of controls; p > 0.01; n = 6), and α2 noradrenergic receptors (increase of 141 ± 15% of controls; p > 0.001; n = 6), respectively. Densities of these receptors were decreased in homozygous animals. Decreases of receptor density in both hetero- and homozygous animals were found for M1 acetylcholine, 5-HT2A serotonin, A2A adenosine, D1 and D2 dopamine, and GABAA receptors, respectively. Other investigated receptor systems showed small changes or were not affected. The present data suggest that the moderate increase of CAG/polyglutamine repeat expansions in the present rat model of Huntington's disease is characterized by subtype-selective and region-specific changes of neuroreceptor densities. In particular, there is evidence for a contribution of predominantly presynaptically localized cholinergic and noradrenergic receptors in the response to Huntington's disease pathology. |
| abstract_unstemmed |
Huntington's disease (HD) is an autosomal dominantly inherited progressive neurodegenerative disorder caused by a CAG/polyglutamine repeat expansion in the gene encoding the huntingtin protein. We have recently generated a rat model transgenic for HD, which displays a slowly progressive phenotype resembling the human adult-onset type of disease. In this study we systematically assessed the distribution and density of 17 transmitter receptors in the brains of 2-year-old rats using quantitative multi-tracer autoradiography and high-resolution positron emission tomography. Heterozygous animals expressed increased densities of M2 acetylcholine (increase of 148 ± 16% of controls; p > 0.001; n = 7), nicotine (increase of 149 ± 16% of controls; p > 0.01; n = 6), and α2 noradrenergic receptors (increase of 141 ± 15% of controls; p > 0.001; n = 6), respectively. Densities of these receptors were decreased in homozygous animals. Decreases of receptor density in both hetero- and homozygous animals were found for M1 acetylcholine, 5-HT2A serotonin, A2A adenosine, D1 and D2 dopamine, and GABAA receptors, respectively. Other investigated receptor systems showed small changes or were not affected. The present data suggest that the moderate increase of CAG/polyglutamine repeat expansions in the present rat model of Huntington's disease is characterized by subtype-selective and region-specific changes of neuroreceptor densities. In particular, there is evidence for a contribution of predominantly presynaptically localized cholinergic and noradrenergic receptors in the response to Huntington's disease pathology. |
| collection_details |
GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE |
| container_issue |
3 |
| title_short |
Regional and subtype selective changes of neurotransmitter receptor density in a rat transgenic for the Huntington's disease mutation |
| url |
http://dx.doi.org/10.1111/j.1471-4159.2005.03169.x |
| remote_bool |
true |
| author2 |
Zilles, Karl Matusch, Andreas Holzmann, Carsten Riess, Olaf Von Hörsten, Stephan |
| author2Str |
Zilles, Karl Matusch, Andreas Holzmann, Carsten Riess, Olaf Von Hörsten, Stephan |
| ppnlink |
NLEJ243927584 |
| mediatype_str_mv |
z |
| isOA_txt |
false |
| hochschulschrift_bool |
false |
| author2_role |
oth oth oth |
| doi_str |
10.1111/j.1471-4159.2005.03169.x |
| up_date |
2024-07-06T04:19:47.926Z |
| _version_ |
1803801946151190528 |
| fullrecord_marcxml |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">NLEJ243113722</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230506005826.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">120427s2005 xx |||||o 00| ||und c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1111/j.1471-4159.2005.03169.x</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)NLEJ243113722</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Bauer, Andreas</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Regional and subtype selective changes of neurotransmitter receptor density in a rat transgenic for the Huntington's disease mutation</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="a">Oxford, UK</subfield><subfield code="b">Blackwell Science Ltd</subfield><subfield code="c">2005</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">Huntington's disease (HD) is an autosomal dominantly inherited progressive neurodegenerative disorder caused by a CAG/polyglutamine repeat expansion in the gene encoding the huntingtin protein. We have recently generated a rat model transgenic for HD, which displays a slowly progressive phenotype resembling the human adult-onset type of disease. In this study we systematically assessed the distribution and density of 17 transmitter receptors in the brains of 2-year-old rats using quantitative multi-tracer autoradiography and high-resolution positron emission tomography. Heterozygous animals expressed increased densities of M2 acetylcholine (increase of 148 ± 16% of controls; p > 0.001; n = 7), nicotine (increase of 149 ± 16% of controls; p > 0.01; n = 6), and α2 noradrenergic receptors (increase of 141 ± 15% of controls; p > 0.001; n = 6), respectively. Densities of these receptors were decreased in homozygous animals. Decreases of receptor density in both hetero- and homozygous animals were found for M1 acetylcholine, 5-HT2A serotonin, A2A adenosine, D1 and D2 dopamine, and GABAA receptors, respectively. Other investigated receptor systems showed small changes or were not affected. The present data suggest that the moderate increase of CAG/polyglutamine repeat expansions in the present rat model of Huntington's disease is characterized by subtype-selective and region-specific changes of neuroreceptor densities. In particular, there is evidence for a contribution of predominantly presynaptically localized cholinergic and noradrenergic receptors in the response to Huntington's disease pathology.</subfield></datafield><datafield tag="533" ind1=" " ind2=" "><subfield code="d">2005</subfield><subfield code="f">Blackwell Publishing Journal Backfiles 1879-2005</subfield><subfield code="7">|2005||||||||||</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Huntington's disease</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Zilles, Karl</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Matusch, Andreas</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Holzmann, Carsten</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Riess, Olaf</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Von Hörsten, Stephan</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">In</subfield><subfield code="t">Journal of neurochemistry</subfield><subfield code="d">Oxford : Wiley-Blackwell, 1956</subfield><subfield code="g">94(2005), 3, Seite 0</subfield><subfield code="h">Online-Ressource</subfield><subfield code="w">(DE-627)NLEJ243927584</subfield><subfield code="w">(DE-600)2020528-4</subfield><subfield code="x">1471-4159</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:94</subfield><subfield code="g">year:2005</subfield><subfield code="g">number:3</subfield><subfield code="g">pages:0</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">http://dx.doi.org/10.1111/j.1471-4159.2005.03169.x</subfield><subfield code="q">text/html</subfield><subfield code="x">Verlag</subfield><subfield code="z">Deutschlandweit zugänglich</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">ZDB-1-DJB</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_NL_ARTICLE</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">94</subfield><subfield code="j">2005</subfield><subfield code="e">3</subfield><subfield code="h">0</subfield></datafield></record></collection>
|
| score |
7.397874 |