Genome-wide microarray analysis identifies a potential role for striatal retrograde endocannabinoid signaling in the pathogenesis of experimental l-DOPA-induced dyskinesia
ABSTRACT l‐3,4‐Dihydroxyphenylalanine (l‐DOPA) is the most widely used drug for the treatment of Parkinson's disease. Unfortunately, chronic administration of this dopamine precursor causes l‐DOPA‐induced dyskinesia (LID), which is a debilitating complication whose pathogenesis remains unclear....
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| Published in | Synapse (New York, N.Y.) Vol. 68; no. 8; pp. 332 - 343 |
|---|---|
| Main Authors | , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Blackwell Publishing Ltd
01.08.2014
Wiley Subscription Services, Inc |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0887-4476 1098-2396 1098-2396 |
| DOI | 10.1002/syn.21740 |
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| Abstract | ABSTRACT
l‐3,4‐Dihydroxyphenylalanine (l‐DOPA) is the most widely used drug for the treatment of Parkinson's disease. Unfortunately, chronic administration of this dopamine precursor causes l‐DOPA‐induced dyskinesia (LID), which is a debilitating complication whose pathogenesis remains unclear. In this study, we compared gene expression profiles of sensorimotor striatum tissue derived from LID and non‐LID 6‐hydroxydopamine‐lesioned rats treated with l‐DOPA. Total RNA was amplified, transcribed and hybridized to Agilent Whole Rat Genome Oligo Microarray chips. Quantitative real‐time reverse transcription PCR was conducted to validate the microarray data. We detected 382 upregulated genes and 115 downregulated genes in LID rats when compared with that of non‐LID subjects with Significance Analysis for Microarrays software. The differentially expressed genes were mainly associated with postsynaptic cell membranes, synapses, and neurotransmitter receptors. Gene Set Analysis (GSA) software was used to identify differentially expressed gene ontology (GO) categories and pathways. The GSA found that “long‐term depression” and “retrograde endocannabinoid signaling” pathways were downregulated, whereas a set of lipid metabolism‐related GO categories and pathways were upregulated in LID rats compared with non‐LID controls. Our study provides further experimental evidence to support the direct correlation between abnormal striatal synaptic plasticity and the induction of LID, and it suggests that the dysfunction of the retrograde endocannabinoid signaling system, a lipid‐based neuromodulatory system, and the relevant alteration of the related lipid metabolism processes might play an important role in the pathogenesis of LID. Synapse 68:332–343, 2014. © 2014 Wiley Periodicals, Inc.
What's new?
The authors compared gene expression profiles of sensorimotor striatum tissue derived from rats with L‐3,4‐dihydroxyphenylalanine (L‐DOPA)‐induced dyskinesia (LID) and non‐LID 6‐hydroxydopamine‐lesioned rats treated with L‐DOPA. The results showed that abnormal striatal synaptic plasticity and the dysfunction of striatal retrograde endocannabinoid signaling might play an important role in the pathogenesis of LID. |
|---|---|
| AbstractList | l-3,4-Dihydroxyphenylalanine (L-DOPA) is the most widely used drug for the treatment of Parkinson's disease. Unfortunately, chronic administration of this dopamine precursor causes L-DOPA-induced dyskinesia (LID), which is a debilitating complication whose pathogenesis remains unclear. In this study, we compared gene expression profiles of sensorimotor striatum tissue derived from LID and non-LID 6-hydroxydopamine-lesioned rats treated with L-DOPA. Total RNA was amplified, transcribed and hybridized to Agilent Whole Rat Genome Oligo Microarray chips. Quantitative real-time reverse transcription PCR was conducted to validate the microarray data. We detected 382 upregulated genes and 115 downregulated genes in LID rats when compared with that of non-LID subjects with Significance Analysis for Microarrays software. The differentially expressed genes were mainly associated with postsynaptic cell membranes, synapses, and neurotransmitter receptors. Gene Set Analysis (GSA) software was used to identify differentially expressed gene ontology (GO) categories and pathways. The GSA found that "long-term depression" and "retrograde endocannabinoid signaling" pathways were downregulated, whereas a set of lipid metabolism-related GO categories and pathways were upregulated in LID rats compared with non-LID controls. Our study provides further experimental evidence to support the direct correlation between abnormal striatal synaptic plasticity and the induction of LID, and it suggests that the dysfunction of the retrograde endocannabinoid signaling system, a lipid-based neuromodulatory system, and the relevant alteration of the related lipid metabolism processes might play an important role in the pathogenesis of LID.l-3,4-Dihydroxyphenylalanine (L-DOPA) is the most widely used drug for the treatment of Parkinson's disease. Unfortunately, chronic administration of this dopamine precursor causes L-DOPA-induced dyskinesia (LID), which is a debilitating complication whose pathogenesis remains unclear. In this study, we compared gene expression profiles of sensorimotor striatum tissue derived from LID and non-LID 6-hydroxydopamine-lesioned rats treated with L-DOPA. Total RNA was amplified, transcribed and hybridized to Agilent Whole Rat Genome Oligo Microarray chips. Quantitative real-time reverse transcription PCR was conducted to validate the microarray data. We detected 382 upregulated genes and 115 downregulated genes in LID rats when compared with that of non-LID subjects with Significance Analysis for Microarrays software. The differentially expressed genes were mainly associated with postsynaptic cell membranes, synapses, and neurotransmitter receptors. Gene Set Analysis (GSA) software was used to identify differentially expressed gene ontology (GO) categories and pathways. The GSA found that "long-term depression" and "retrograde endocannabinoid signaling" pathways were downregulated, whereas a set of lipid metabolism-related GO categories and pathways were upregulated in LID rats compared with non-LID controls. Our study provides further experimental evidence to support the direct correlation between abnormal striatal synaptic plasticity and the induction of LID, and it suggests that the dysfunction of the retrograde endocannabinoid signaling system, a lipid-based neuromodulatory system, and the relevant alteration of the related lipid metabolism processes might play an important role in the pathogenesis of LID. l-3,4-Dihydroxyphenylalanine (l-DOPA) is the most widely used drug for the treatment of Parkinson's disease. Unfortunately, chronic administration of this dopamine precursor causes l-DOPA-induced dyskinesia (LID), which is a debilitating complication whose pathogenesis remains unclear. In this study, we compared gene expression profiles of sensorimotor striatum tissue derived from LID and non-LID 6-hydroxydopamine-lesioned rats treated with l-DOPA. Total RNA was amplified, transcribed and hybridized to Agilent Whole Rat Genome Oligo Microarray chips. Quantitative real-time reverse transcription PCR was conducted to validate the microarray data. We detected 382 upregulated genes and 115 downregulated genes in LID rats when compared with that of non-LID subjects with Significance Analysis for Microarrays software. The differentially expressed genes were mainly associated with postsynaptic cell membranes, synapses, and neurotransmitter receptors. Gene Set Analysis (GSA) software was used to identify differentially expressed gene ontology (GO) categories and pathways. The GSA found that "long-term depression" and "retrograde endocannabinoid signaling" pathways were downregulated, whereas a set of lipid metabolism-related GO categories and pathways were upregulated in LID rats compared with non-LID controls. Our study provides further experimental evidence to support the direct correlation between abnormal striatal synaptic plasticity and the induction of LID, and it suggests that the dysfunction of the retrograde endocannabinoid signaling system, a lipid-based neuromodulatory system, and the relevant alteration of the related lipid metabolism processes might play an important role in the pathogenesis of LID. Synapse 68:332-343, 2014. copyright 2014 Wiley Periodicals, Inc. What's new? The authors compared gene expression profiles of sensorimotor striatum tissue derived from rats with L-3,4-dihydroxyphenylalanine (L-DOPA)-induced dyskinesia (LID) and non-LID 6-hydroxydopamine-lesioned rats treated with L-DOPA. The results showed that abnormal striatal synaptic plasticity and the dysfunction of striatal retrograde endocannabinoid signaling might play an important role in the pathogenesis of LID. l-3,4-Dihydroxyphenylalanine (L-DOPA) is the most widely used drug for the treatment of Parkinson's disease. Unfortunately, chronic administration of this dopamine precursor causes L-DOPA-induced dyskinesia (LID), which is a debilitating complication whose pathogenesis remains unclear. In this study, we compared gene expression profiles of sensorimotor striatum tissue derived from LID and non-LID 6-hydroxydopamine-lesioned rats treated with L-DOPA. Total RNA was amplified, transcribed and hybridized to Agilent Whole Rat Genome Oligo Microarray chips. Quantitative real-time reverse transcription PCR was conducted to validate the microarray data. We detected 382 upregulated genes and 115 downregulated genes in LID rats when compared with that of non-LID subjects with Significance Analysis for Microarrays software. The differentially expressed genes were mainly associated with postsynaptic cell membranes, synapses, and neurotransmitter receptors. Gene Set Analysis (GSA) software was used to identify differentially expressed gene ontology (GO) categories and pathways. The GSA found that "long-term depression" and "retrograde endocannabinoid signaling" pathways were downregulated, whereas a set of lipid metabolism-related GO categories and pathways were upregulated in LID rats compared with non-LID controls. Our study provides further experimental evidence to support the direct correlation between abnormal striatal synaptic plasticity and the induction of LID, and it suggests that the dysfunction of the retrograde endocannabinoid signaling system, a lipid-based neuromodulatory system, and the relevant alteration of the related lipid metabolism processes might play an important role in the pathogenesis of LID. l ‐3,4‐Dihydroxyphenylalanine ( l ‐DOPA) is the most widely used drug for the treatment of Parkinson's disease. Unfortunately, chronic administration of this dopamine precursor causes l ‐DOPA‐induced dyskinesia (LID), which is a debilitating complication whose pathogenesis remains unclear. In this study, we compared gene expression profiles of sensorimotor striatum tissue derived from LID and non‐LID 6‐hydroxydopamine‐lesioned rats treated with l ‐DOPA. Total RNA was amplified, transcribed and hybridized to Agilent Whole Rat Genome Oligo Microarray chips. Quantitative real‐time reverse transcription PCR was conducted to validate the microarray data. We detected 382 upregulated genes and 115 downregulated genes in LID rats when compared with that of non‐LID subjects with Significance Analysis for Microarrays software. The differentially expressed genes were mainly associated with postsynaptic cell membranes, synapses, and neurotransmitter receptors. Gene Set Analysis (GSA) software was used to identify differentially expressed gene ontology (GO) categories and pathways. The GSA found that “long‐term depression” and “retrograde endocannabinoid signaling” pathways were downregulated, whereas a set of lipid metabolism‐related GO categories and pathways were upregulated in LID rats compared with non‐LID controls. Our study provides further experimental evidence to support the direct correlation between abnormal striatal synaptic plasticity and the induction of LID, and it suggests that the dysfunction of the retrograde endocannabinoid signaling system, a lipid‐based neuromodulatory system, and the relevant alteration of the related lipid metabolism processes might play an important role in the pathogenesis of LID. Synapse 68:332–343, 2014. © 2014 Wiley Periodicals, Inc. l-3,4-Dihydroxyphenylalanine (l-DOPA) is the most widely used drug for the treatment of Parkinson's disease. Unfortunately, chronic administration of this dopamine precursor causes l-DOPA-induced dyskinesia (LID), which is a debilitating complication whose pathogenesis remains unclear. In this study, we compared gene expression profiles of sensorimotor striatum tissue derived from LID and non-LID 6-hydroxydopamine-lesioned rats treated with l-DOPA. Total RNA was amplified, transcribed and hybridized to Agilent Whole Rat Genome Oligo Microarray chips. Quantitative real-time reverse transcription PCR was conducted to validate the microarray data. We detected 382 upregulated genes and 115 downregulated genes in LID rats when compared with that of non-LID subjects with Significance Analysis for Microarrays software. The differentially expressed genes were mainly associated with postsynaptic cell membranes, synapses, and neurotransmitter receptors. Gene Set Analysis (GSA) software was used to identify differentially expressed gene ontology (GO) categories and pathways. The GSA found that "long-term depression" and "retrograde endocannabinoid signaling" pathways were downregulated, whereas a set of lipid metabolism-related GO categories and pathways were upregulated in LID rats compared with non-LID controls. Our study provides further experimental evidence to support the direct correlation between abnormal striatal synaptic plasticity and the induction of LID, and it suggests that the dysfunction of the retrograde endocannabinoid signaling system, a lipid-based neuromodulatory system, and the relevant alteration of the related lipid metabolism processes might play an important role in the pathogenesis of LID. Synapse 68:332-343, 2014. © 2014 Wiley Periodicals, Inc. [PUBLICATION ABSTRACT] ABSTRACT l‐3,4‐Dihydroxyphenylalanine (l‐DOPA) is the most widely used drug for the treatment of Parkinson's disease. Unfortunately, chronic administration of this dopamine precursor causes l‐DOPA‐induced dyskinesia (LID), which is a debilitating complication whose pathogenesis remains unclear. In this study, we compared gene expression profiles of sensorimotor striatum tissue derived from LID and non‐LID 6‐hydroxydopamine‐lesioned rats treated with l‐DOPA. Total RNA was amplified, transcribed and hybridized to Agilent Whole Rat Genome Oligo Microarray chips. Quantitative real‐time reverse transcription PCR was conducted to validate the microarray data. We detected 382 upregulated genes and 115 downregulated genes in LID rats when compared with that of non‐LID subjects with Significance Analysis for Microarrays software. The differentially expressed genes were mainly associated with postsynaptic cell membranes, synapses, and neurotransmitter receptors. Gene Set Analysis (GSA) software was used to identify differentially expressed gene ontology (GO) categories and pathways. The GSA found that “long‐term depression” and “retrograde endocannabinoid signaling” pathways were downregulated, whereas a set of lipid metabolism‐related GO categories and pathways were upregulated in LID rats compared with non‐LID controls. Our study provides further experimental evidence to support the direct correlation between abnormal striatal synaptic plasticity and the induction of LID, and it suggests that the dysfunction of the retrograde endocannabinoid signaling system, a lipid‐based neuromodulatory system, and the relevant alteration of the related lipid metabolism processes might play an important role in the pathogenesis of LID. Synapse 68:332–343, 2014. © 2014 Wiley Periodicals, Inc. What's new? The authors compared gene expression profiles of sensorimotor striatum tissue derived from rats with L‐3,4‐dihydroxyphenylalanine (L‐DOPA)‐induced dyskinesia (LID) and non‐LID 6‐hydroxydopamine‐lesioned rats treated with L‐DOPA. The results showed that abnormal striatal synaptic plasticity and the dysfunction of striatal retrograde endocannabinoid signaling might play an important role in the pathogenesis of LID. |
| Author | Liu, Jian Zhang, Qiao Jun Wang, Tao Wang, Hui Sheng Wang, Yong |
| Author_xml | – sequence: 1 givenname: Yong surname: Wang fullname: Wang, Yong organization: Department of Physiology and Pathophysiology, School of Medicine, Xi'an Jiaotong University, 710061, Xi'an, China – sequence: 2 givenname: Qiao Jun surname: Zhang fullname: Zhang, Qiao Jun organization: Department of Rehabilitation Medicine, The Second Hospital, Xi'an Jiaotong University, 710004, Xi'an, China – sequence: 3 givenname: Hui Sheng surname: Wang fullname: Wang, Hui Sheng organization: Department of Physiology and Pathophysiology, School of Medicine, Xi'an Jiaotong University, 710061, Xi'an, China – sequence: 4 givenname: Tao surname: Wang fullname: Wang, Tao organization: Department of Physiology and Pathophysiology, School of Medicine, Xi'an Jiaotong University, 710061, Xi'an, China – sequence: 5 givenname: Jian surname: Liu fullname: Liu, Jian email: liujian@mail.xjtu.edu.cn organization: Department of Physiology and Pathophysiology, School of Medicine, Xi'an Jiaotong University, 710061, Xi'an, China |
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| Keywords | l-DOPA endocannabinoid microarray Parkinson's disease dyskinesia |
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Metabotropic glutama 2009; 89 2012; 122 2010; 13 2000; 47 2002; 10 2011; 61 2008; 9 2003; 18 2000; 28(1) 1998; 83 2007; 30 2013; 8 2001; 85 2003; 110 2005; 25 2009; 56 2012; 72 2013; 79C 2000; 14 2003; 6 2010; 112 2000; 62 2008; 119 2008; 23 2007; 6 2008; 64 2007; 1 2001; 14 2012; 20 2010; 9 2001; 98 2010; 1324 2000; 25 2002; 175 2002; 5 2006; 5 2006; 3 2005 2007; 208 2011; 6 2012; 76 2011; 134 2001; 21 2004; 17 2006; 48 2002; 66 2005; 6 2001; 2 1957; 180 2009; 4 2008; 211 2012; 7 e_1_2_6_51_1 e_1_2_6_53_1 e_1_2_6_32_1 e_1_2_6_30_1 Paxinos G (e_1_2_6_46_1) 2005 e_1_2_6_19_1 e_1_2_6_13_1 e_1_2_6_36_1 e_1_2_6_11_1 e_1_2_6_34_1 e_1_2_6_17_1 e_1_2_6_55_1 e_1_2_6_15_1 e_1_2_6_38_1 e_1_2_6_43_1 e_1_2_6_41_1 e_1_2_6_5_1 e_1_2_6_7_1 e_1_2_6_24_1 e_1_2_6_49_1 e_1_2_6_3_1 e_1_2_6_22_1 e_1_2_6_28_1 e_1_2_6_45_1 e_1_2_6_26_1 e_1_2_6_47_1 M Kanehisa (e_1_2_6_31_1) 2000; 28 e_1_2_6_52_1 e_1_2_6_54_1 e_1_2_6_10_1 Marzo V (e_1_2_6_18_1) 2000; 14 e_1_2_6_50_1 Fahn S (e_1_2_6_20_1) 2000; 47 Bonaventura J (e_1_2_6_9_1) 2013; 79 e_1_2_6_14_1 e_1_2_6_35_1 e_1_2_6_12_1 e_1_2_6_33_1 e_1_2_6_39_1 e_1_2_6_16_1 e_1_2_6_37_1 e_1_2_6_42_1 e_1_2_6_21_1 e_1_2_6_40_1 e_1_2_6_8_1 e_1_2_6_4_1 e_1_2_6_6_1 e_1_2_6_25_1 e_1_2_6_48_1 e_1_2_6_23_1 e_1_2_6_2_1 e_1_2_6_29_1 e_1_2_6_44_1 e_1_2_6_27_1 |
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l‐3,4‐Dihydroxyphenylalanine (l‐DOPA) is the most widely used drug for the treatment of Parkinson's disease. Unfortunately, chronic administration of... l ‐3,4‐Dihydroxyphenylalanine ( l ‐DOPA) is the most widely used drug for the treatment of Parkinson's disease. Unfortunately, chronic administration of this... l-3,4-Dihydroxyphenylalanine (L-DOPA) is the most widely used drug for the treatment of Parkinson's disease. Unfortunately, chronic administration of this... l-3,4-Dihydroxyphenylalanine (l-DOPA) is the most widely used drug for the treatment of Parkinson's disease. Unfortunately, chronic administration of this... |
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| SubjectTerms | Adrenergic Agents - toxicity Animals Antiparkinson Agents - adverse effects Corpus Striatum - drug effects Corpus Striatum - physiopathology dyskinesia Dyskinesia, Drug-Induced - physiopathology endocannabinoid Endocannabinoids - metabolism Gene Expression - drug effects Gene Ontology l-DOPA Levodopa - adverse effects Male microarray Microarray Analysis Motor Activity - drug effects Motor Activity - physiology Oxidopamine - toxicity Parkinson's disease Rats, Sprague-Dawley Real-Time Polymerase Chain Reaction Reverse Transcriptase Polymerase Chain Reaction Signal Transduction - drug effects |
| Title | Genome-wide microarray analysis identifies a potential role for striatal retrograde endocannabinoid signaling in the pathogenesis of experimental l-DOPA-induced dyskinesia |
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