Differential modulation of dopamine D 1 -receptor binding and mRNA expression in the basal ganglia by the D 1 -receptor antagonist, SCH-23390
Dopamine D 1 -receptor binding in the basal ganglia is differentially regulated by subtype nonspecific dopamine antagonists such as the antipsychotic, Fluphenazine. The purpose of the present study was to determine the relative contributions of D 1 and D 2 receptor systems in the regulation of basal...
Guardado en:
Publicado: |
1998
|
---|---|
Materias: | |
Acceso en línea: | https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_08874476_v30_n1_p38_Yu http://hdl.handle.net/20.500.12110/paper_08874476_v30_n1_p38_Yu |
Aporte de: |
id |
paper:paper_08874476_v30_n1_p38_Yu |
---|---|
record_format |
dspace |
spelling |
paper:paper_08874476_v30_n1_p38_Yu2023-06-08T15:46:49Z Differential modulation of dopamine D 1 -receptor binding and mRNA expression in the basal ganglia by the D 1 -receptor antagonist, SCH-23390 D 2 - receptor Entopeduncular nucleus Parkinson's disease Substantia nigra Subthalamic nucleus 8 chloro 2,3,4,5 tetrahydro 3 methyl 5 phenyl 1h 3 benzazepin 7 ol hydrogen maleate dopamine 1 receptor n [(1 ethyl 2 pyrrolidinyl)methyl] 3 iodo 5,6 dimethoxysalicylamide raclopride animal experiment animal tissue article controlled study dopaminergic nerve cell drug effect drug receptor binding female nonhuman parkinson disease priority journal rat receptor binding subcutaneous drug administration (R)-2,3,4,5-Tetrahydro-8-chloro-3-methyl-5-phenyl-1H-3-benzazepin-7-ol Animals Autoradiography Basal Ganglia Dopamine Antagonists Female Gene Expression Regulation Iodine Radioisotopes Kinetics Raclopride Rats Rats, Sprague-Dawley Receptors, Dopamine D1 RNA, Messenger Salicylamides Substantia Nigra Transcription, Genetic Dopamine D 1 -receptor binding in the basal ganglia is differentially regulated by subtype nonspecific dopamine antagonists such as the antipsychotic, Fluphenazine. The purpose of the present study was to determine the relative contributions of D 1 and D 2 receptor systems in the regulation of basal ganglia D 1 -receptor binding. Rats were injected twice daily for 21 days with saline, the D 1 -receptor antagonist, SCH-23390, the D 2 -receptor antagonist, Raclopride, or both SCH-23390 and Raclopride. Dopamine D 1 -receptor levels (as indicated by [ 125 I]SCH-23982 binding) and mRNA expression were measured using receptor autoradiographic and in situ hybridization histochemical techniques. [ 125 I]NCQ-298 binding to D 2 - receptors was also measured as a positive control for the effects of Raclopride. SCH-23390 administration independently increased [ 125 I]SCH- 23982 binding in a region-dependent manner with the greatest increases occurring in the entopeduncular nucleus. SCH-23390 also increased D 1 - receptor mRNA expression in specific striatal subregions suggesting that increases in binding were related to changes in receptor synthesis. In addition, Raclopride independently enhanced D 2 binding with comparable increases observed in extrastriatal regions and increases of a lesser magnitude in the striatum. These data show that the modulation of basal ganglia D 1 -receptor binding observed in animals treated with nonselective antagonists is due primarily to the blockade of D 1 -receptors. The differential enhancement in basal ganglia D 1 binding observed after D 1 - receptor blockade may be due to anatomical or phenotypic heterogeneity within the population of striatal D 1 -receptor synthesizing neurons. Similarly, the differential enhancement in striatal and extrastriatal D 2 -receptor binding may be due to differences in the regulation of striatal and extrastriatal D 2 -receptor synthesizing neurons. 1998 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_08874476_v30_n1_p38_Yu http://hdl.handle.net/20.500.12110/paper_08874476_v30_n1_p38_Yu |
institution |
Universidad de Buenos Aires |
institution_str |
I-28 |
repository_str |
R-134 |
collection |
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) |
topic |
D 2 - receptor Entopeduncular nucleus Parkinson's disease Substantia nigra Subthalamic nucleus 8 chloro 2,3,4,5 tetrahydro 3 methyl 5 phenyl 1h 3 benzazepin 7 ol hydrogen maleate dopamine 1 receptor n [(1 ethyl 2 pyrrolidinyl)methyl] 3 iodo 5,6 dimethoxysalicylamide raclopride animal experiment animal tissue article controlled study dopaminergic nerve cell drug effect drug receptor binding female nonhuman parkinson disease priority journal rat receptor binding subcutaneous drug administration (R)-2,3,4,5-Tetrahydro-8-chloro-3-methyl-5-phenyl-1H-3-benzazepin-7-ol Animals Autoradiography Basal Ganglia Dopamine Antagonists Female Gene Expression Regulation Iodine Radioisotopes Kinetics Raclopride Rats Rats, Sprague-Dawley Receptors, Dopamine D1 RNA, Messenger Salicylamides Substantia Nigra Transcription, Genetic |
spellingShingle |
D 2 - receptor Entopeduncular nucleus Parkinson's disease Substantia nigra Subthalamic nucleus 8 chloro 2,3,4,5 tetrahydro 3 methyl 5 phenyl 1h 3 benzazepin 7 ol hydrogen maleate dopamine 1 receptor n [(1 ethyl 2 pyrrolidinyl)methyl] 3 iodo 5,6 dimethoxysalicylamide raclopride animal experiment animal tissue article controlled study dopaminergic nerve cell drug effect drug receptor binding female nonhuman parkinson disease priority journal rat receptor binding subcutaneous drug administration (R)-2,3,4,5-Tetrahydro-8-chloro-3-methyl-5-phenyl-1H-3-benzazepin-7-ol Animals Autoradiography Basal Ganglia Dopamine Antagonists Female Gene Expression Regulation Iodine Radioisotopes Kinetics Raclopride Rats Rats, Sprague-Dawley Receptors, Dopamine D1 RNA, Messenger Salicylamides Substantia Nigra Transcription, Genetic Differential modulation of dopamine D 1 -receptor binding and mRNA expression in the basal ganglia by the D 1 -receptor antagonist, SCH-23390 |
topic_facet |
D 2 - receptor Entopeduncular nucleus Parkinson's disease Substantia nigra Subthalamic nucleus 8 chloro 2,3,4,5 tetrahydro 3 methyl 5 phenyl 1h 3 benzazepin 7 ol hydrogen maleate dopamine 1 receptor n [(1 ethyl 2 pyrrolidinyl)methyl] 3 iodo 5,6 dimethoxysalicylamide raclopride animal experiment animal tissue article controlled study dopaminergic nerve cell drug effect drug receptor binding female nonhuman parkinson disease priority journal rat receptor binding subcutaneous drug administration (R)-2,3,4,5-Tetrahydro-8-chloro-3-methyl-5-phenyl-1H-3-benzazepin-7-ol Animals Autoradiography Basal Ganglia Dopamine Antagonists Female Gene Expression Regulation Iodine Radioisotopes Kinetics Raclopride Rats Rats, Sprague-Dawley Receptors, Dopamine D1 RNA, Messenger Salicylamides Substantia Nigra Transcription, Genetic |
description |
Dopamine D 1 -receptor binding in the basal ganglia is differentially regulated by subtype nonspecific dopamine antagonists such as the antipsychotic, Fluphenazine. The purpose of the present study was to determine the relative contributions of D 1 and D 2 receptor systems in the regulation of basal ganglia D 1 -receptor binding. Rats were injected twice daily for 21 days with saline, the D 1 -receptor antagonist, SCH-23390, the D 2 -receptor antagonist, Raclopride, or both SCH-23390 and Raclopride. Dopamine D 1 -receptor levels (as indicated by [ 125 I]SCH-23982 binding) and mRNA expression were measured using receptor autoradiographic and in situ hybridization histochemical techniques. [ 125 I]NCQ-298 binding to D 2 - receptors was also measured as a positive control for the effects of Raclopride. SCH-23390 administration independently increased [ 125 I]SCH- 23982 binding in a region-dependent manner with the greatest increases occurring in the entopeduncular nucleus. SCH-23390 also increased D 1 - receptor mRNA expression in specific striatal subregions suggesting that increases in binding were related to changes in receptor synthesis. In addition, Raclopride independently enhanced D 2 binding with comparable increases observed in extrastriatal regions and increases of a lesser magnitude in the striatum. These data show that the modulation of basal ganglia D 1 -receptor binding observed in animals treated with nonselective antagonists is due primarily to the blockade of D 1 -receptors. The differential enhancement in basal ganglia D 1 binding observed after D 1 - receptor blockade may be due to anatomical or phenotypic heterogeneity within the population of striatal D 1 -receptor synthesizing neurons. Similarly, the differential enhancement in striatal and extrastriatal D 2 -receptor binding may be due to differences in the regulation of striatal and extrastriatal D 2 -receptor synthesizing neurons. |
title |
Differential modulation of dopamine D 1 -receptor binding and mRNA expression in the basal ganglia by the D 1 -receptor antagonist, SCH-23390 |
title_short |
Differential modulation of dopamine D 1 -receptor binding and mRNA expression in the basal ganglia by the D 1 -receptor antagonist, SCH-23390 |
title_full |
Differential modulation of dopamine D 1 -receptor binding and mRNA expression in the basal ganglia by the D 1 -receptor antagonist, SCH-23390 |
title_fullStr |
Differential modulation of dopamine D 1 -receptor binding and mRNA expression in the basal ganglia by the D 1 -receptor antagonist, SCH-23390 |
title_full_unstemmed |
Differential modulation of dopamine D 1 -receptor binding and mRNA expression in the basal ganglia by the D 1 -receptor antagonist, SCH-23390 |
title_sort |
differential modulation of dopamine d 1 -receptor binding and mrna expression in the basal ganglia by the d 1 -receptor antagonist, sch-23390 |
publishDate |
1998 |
url |
https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_08874476_v30_n1_p38_Yu http://hdl.handle.net/20.500.12110/paper_08874476_v30_n1_p38_Yu |
_version_ |
1768541758850859008 |