Delayed Treatment of Capsaicin Produces Partial Motor Recovery by Enhancing Dopamine Function in MPP + -lesioned Rats via Ciliary Neurotrophic Factor
Transient receptor potential vanilloid subtype 1 (TRPV1) on astrocytes prevents ongoing degeneration of nigrostriatal dopamine (DA) neurons in MPP -lesioned rats via ciliary neurotrophic factor (CNTF). The present study determined whether such a beneficial effect of astrocytic TRPV1 could be achieve...
Saved in:
| Published in | Experimental neurobiology Vol. 28; no. 2; pp. 289 - 299 |
|---|---|
| Main Authors | , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Korea (South)
The Korean Society for Brain and Neural Science
01.04.2019
한국뇌신경과학회 |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1226-2560 2093-8144 2093-8144 |
| DOI | 10.5607/en.2019.28.2.289 |
Cover
| Abstract | Transient receptor potential vanilloid subtype 1 (TRPV1) on astrocytes prevents ongoing degeneration of nigrostriatal dopamine (DA) neurons in MPP
-lesioned rats via ciliary neurotrophic factor (CNTF). The present study determined whether such a beneficial effect of astrocytic TRPV1 could be achieved after completion of injury of DA neurons, rather than ongoing injury, which seems more relevant to therapeutics. To test this, the MPP
-lesioned rat model utilized here exhibited approximately 70~80% degeneration of nigrostriatal DA neurons that was completed at 2 weeks post medial forebrain bundle injection of MPP
. TRPV1 agonist, capsaicin (CAP), was intraperitoneally administered. CNTF receptor alpha neutralizing antibody (CNTFRαNAb) was nigral injected to evaluate the role of CNTF endogenously produced by astrocyte through TRPV1 activation on DA neurons. Delayed treatment of CAP produced a significant reduction in amphetamine-induced rotational asymmetry. Accompanying this behavioral recovery, CAP treatment increased CNTF levels and tyrosine hydroxylase (TH) activity in the substantia nigra pars compacta (SNpc), and levels of DA and its metabolites in the striatum compared to controls. Interestingly, behavioral recovery and increases in biochemical indices were not reflected in trophic changes of the DA system. Instead, behavioral recovery was temporal and dependent on the continuous presence of CAP treatment. The results suggest that delayed treatment of CAP increases nigral TH enzyme activity and striatal levels of DA and its metabolites by CNTF endogenously derived from CAP-activated astrocytes through TRPV1, leading to functional recovery. Consequently, these findings may be useful in the treatment of DA imbalances associated with Parkinson's disease. |
|---|---|
| AbstractList | Transient receptor potential vanilloid subtype 1 (TRPV1) on astrocytes prevents ongoing degeneration of nigrostriatal dopamine (DA) neurons in MPP+-lesioned rats via ciliary neurotrophic factor (CNTF). The present study determined whether such a beneficial effect of astrocytic TRPV1 could be achieved after completion of injury of DA neurons, rather than ongoing injury, which seems more relevant to therapeutics. To test this, the MPP+-lesioned rat model utilized here exhibited approximately 70~80% degeneration of nigrostriatal DA neurons that was completed at 2 weeks post medial forebrain bundle injection of MPP+. TRPV1 agonist, capsaicin (CAP), was intraperitoneally administered. CNTF receptor alpha neutralizing antibody (CNTFRαNAb) was nigral injected to evaluate the role of CNTF endogenously produced by astrocyte through TRPV1 activation on DA neurons. Delayed treatment of CAP produced a significant reduction in amphetamine-induced rotational asymmetry. Accompanying this behavioral recovery, CAP treatment increased CNTF levels and tyrosine hydroxylase (TH) activity in the substantia nigra pars compacta (SNpc), and levels of DA and its metabolites in the striatum compared to controls. Interestingly, behavioral recovery and increases in biochemical indices were not reflected in trophic changes of the DA system. Instead, behavioral recovery was temporal and dependent on the continuous presence of CAP treatment. The results suggest that delayed treatment of CAP increases nigral TH enzyme activity and striatal levels of DA and its metabolites by CNTF endogenously derived from CAP-activated astrocytes through TRPV1, leading to functional recovery. Consequently, these findings may be useful in the treatment of DA imbalances associated with Parkinson’s disease. KCI Citation Count: 0 Transient receptor potential vanilloid subtype 1 (TRPV1) on astrocytes prevents ongoing degeneration of nigrostriatal dopamine (DA) neurons in MPP+-lesioned rats via ciliary neurotrophic factor (CNTF). The present study determined whether such a beneficial effect of astrocytic TRPV1 could be achieved after completion of injury of DA neurons, rather than ongoing injury, which seems more relevant to therapeutics. To test this, the MPP+-lesioned rat model utilized here exhibited approximately 70~80% degeneration of nigrostriatal DA neurons that was completed at 2 weeks post medial forebrain bundle injection of MPP+. TRPV1 agonist, capsaicin (CAP), was intraperitoneally administered. CNTF receptor alpha neutralizing antibody (CNTFRαNAb) was nigral injected to evaluate the role of CNTF endogenously produced by astrocyte through TRPV1 activation on DA neurons. Delayed treatment of CAP produced a significant reduction in amphetamine-induced rotational asymmetry. Accompanying this behavioral recovery, CAP treatment increased CNTF levels and tyrosine hydroxylase (TH) activity in the substantia nigra pars compacta (SNpc), and levels of DA and its metabolites in the striatum compared to controls. Interestingly, behavioral recovery and increases in biochemical indices were not reflected in trophic changes of the DA system. Instead, behavioral recovery was temporal and dependent on the continuous presence of CAP treatment. The results suggest that delayed treatment of CAP increases nigral TH enzyme activity and striatal levels of DA and its metabolites by CNTF endogenously derived from CAP-activated astrocytes through TRPV1, leading to functional recovery. Consequently, these findings may be useful in the treatment of DA imbalances associated with Parkinson's disease. Transient receptor potential vanilloid subtype 1 (TRPV1) on astrocytes prevents ongoing degeneration of nigrostriatal dopamine (DA) neurons in MPP -lesioned rats via ciliary neurotrophic factor (CNTF). The present study determined whether such a beneficial effect of astrocytic TRPV1 could be achieved after completion of injury of DA neurons, rather than ongoing injury, which seems more relevant to therapeutics. To test this, the MPP -lesioned rat model utilized here exhibited approximately 70~80% degeneration of nigrostriatal DA neurons that was completed at 2 weeks post medial forebrain bundle injection of MPP . TRPV1 agonist, capsaicin (CAP), was intraperitoneally administered. CNTF receptor alpha neutralizing antibody (CNTFRαNAb) was nigral injected to evaluate the role of CNTF endogenously produced by astrocyte through TRPV1 activation on DA neurons. Delayed treatment of CAP produced a significant reduction in amphetamine-induced rotational asymmetry. Accompanying this behavioral recovery, CAP treatment increased CNTF levels and tyrosine hydroxylase (TH) activity in the substantia nigra pars compacta (SNpc), and levels of DA and its metabolites in the striatum compared to controls. Interestingly, behavioral recovery and increases in biochemical indices were not reflected in trophic changes of the DA system. Instead, behavioral recovery was temporal and dependent on the continuous presence of CAP treatment. The results suggest that delayed treatment of CAP increases nigral TH enzyme activity and striatal levels of DA and its metabolites by CNTF endogenously derived from CAP-activated astrocytes through TRPV1, leading to functional recovery. Consequently, these findings may be useful in the treatment of DA imbalances associated with Parkinson's disease. Transient receptor potential vanilloid subtype 1 (TRPV1) on astrocytes prevents ongoing degeneration of nigrostriatal dopamine (DA) neurons in MPP+-lesioned rats via ciliary neurotrophic factor (CNTF). The present study determined whether such a beneficial effect of astrocytic TRPV1 could be achieved after completion of injury of DA neurons, rather than ongoing injury, which seems more relevant to therapeutics. To test this, the MPP+-lesioned rat model utilized here exhibited approximately 70~80% degeneration of nigrostriatal DA neurons that was completed at 2 weeks post medial forebrain bundle injection of MPP+. TRPV1 agonist, capsaicin (CAP), was intraperitoneally administered. CNTF receptor alpha neutralizing antibody (CNTFRαNAb) was nigral injected to evaluate the role of CNTF endogenously produced by astrocyte through TRPV1 activation on DA neurons. Delayed treatment of CAP produced a significant reduction in amphetamine-induced rotational asymmetry. Accompanying this behavioral recovery, CAP treatment increased CNTF levels and tyrosine hydroxylase (TH) activity in the substantia nigra pars compacta (SNpc), and levels of DA and its metabolites in the striatum compared to controls. Interestingly, behavioral recovery and increases in biochemical indices were not reflected in trophic changes of the DA system. Instead, behavioral recovery was temporal and dependent on the continuous presence of CAP treatment. The results suggest that delayed treatment of CAP increases nigral TH enzyme activity and striatal levels of DA and its metabolites by CNTF endogenously derived from CAP-activated astrocytes through TRPV1, leading to functional recovery. Consequently, these findings may be useful in the treatment of DA imbalances associated with Parkinson's disease.Transient receptor potential vanilloid subtype 1 (TRPV1) on astrocytes prevents ongoing degeneration of nigrostriatal dopamine (DA) neurons in MPP+-lesioned rats via ciliary neurotrophic factor (CNTF). The present study determined whether such a beneficial effect of astrocytic TRPV1 could be achieved after completion of injury of DA neurons, rather than ongoing injury, which seems more relevant to therapeutics. To test this, the MPP+-lesioned rat model utilized here exhibited approximately 70~80% degeneration of nigrostriatal DA neurons that was completed at 2 weeks post medial forebrain bundle injection of MPP+. TRPV1 agonist, capsaicin (CAP), was intraperitoneally administered. CNTF receptor alpha neutralizing antibody (CNTFRαNAb) was nigral injected to evaluate the role of CNTF endogenously produced by astrocyte through TRPV1 activation on DA neurons. Delayed treatment of CAP produced a significant reduction in amphetamine-induced rotational asymmetry. Accompanying this behavioral recovery, CAP treatment increased CNTF levels and tyrosine hydroxylase (TH) activity in the substantia nigra pars compacta (SNpc), and levels of DA and its metabolites in the striatum compared to controls. Interestingly, behavioral recovery and increases in biochemical indices were not reflected in trophic changes of the DA system. Instead, behavioral recovery was temporal and dependent on the continuous presence of CAP treatment. The results suggest that delayed treatment of CAP increases nigral TH enzyme activity and striatal levels of DA and its metabolites by CNTF endogenously derived from CAP-activated astrocytes through TRPV1, leading to functional recovery. Consequently, these findings may be useful in the treatment of DA imbalances associated with Parkinson's disease. |
| Author | Baek, Jeong Yeob Jeong, Jae Yeong Park, Eun Su Bok, Eugene Chung, Young Cheul Nam, Jin Han Shin, Won-Ho Jin, Byung Kwan Kim, Kyoung In |
| AuthorAffiliation | 1 Department of Neuroscience, Graduate School, Kyung Hee University, Seoul 02447, Korea 2 Department of Biochemistry & Molecular Biology, School of Medicine, Kyung Hee University, Seoul 02447, Korea 3 Department of Predictive Toxicology, Korea Institute of Toxicology, Daejeon 34114, Korea |
| AuthorAffiliation_xml | – name: 2 Department of Biochemistry & Molecular Biology, School of Medicine, Kyung Hee University, Seoul 02447, Korea – name: 1 Department of Neuroscience, Graduate School, Kyung Hee University, Seoul 02447, Korea – name: 3 Department of Predictive Toxicology, Korea Institute of Toxicology, Daejeon 34114, Korea |
| Author_xml | – sequence: 1 givenname: Kyoung In surname: Kim fullname: Kim, Kyoung In organization: Department of Neuroscience, Graduate School, Kyung Hee University, Seoul 02447, Korea – sequence: 2 givenname: Jeong Yeob surname: Baek fullname: Baek, Jeong Yeob organization: Department of Neuroscience, Graduate School, Kyung Hee University, Seoul 02447, Korea – sequence: 3 givenname: Jae Yeong surname: Jeong fullname: Jeong, Jae Yeong organization: Department of Neuroscience, Graduate School, Kyung Hee University, Seoul 02447, Korea – sequence: 4 givenname: Jin Han surname: Nam fullname: Nam, Jin Han organization: Department of Neuroscience, Graduate School, Kyung Hee University, Seoul 02447, Korea – sequence: 5 givenname: Eun Su surname: Park fullname: Park, Eun Su organization: Department of Neuroscience, Graduate School, Kyung Hee University, Seoul 02447, Korea – sequence: 6 givenname: Eugene surname: Bok fullname: Bok, Eugene organization: Department of Predictive Toxicology, Korea Institute of Toxicology, Daejeon 34114, Korea – sequence: 7 givenname: Won-Ho surname: Shin fullname: Shin, Won-Ho organization: Department of Predictive Toxicology, Korea Institute of Toxicology, Daejeon 34114, Korea – sequence: 8 givenname: Young Cheul surname: Chung fullname: Chung, Young Cheul organization: Department of Biochemistry & Molecular Biology, School of Medicine, Kyung Hee University, Seoul 02447, Korea – sequence: 9 givenname: Byung Kwan surname: Jin fullname: Jin, Byung Kwan organization: Department of Neuroscience, Graduate School, Kyung Hee University, Seoul 02447, Korea, Department of Biochemistry & Molecular Biology, School of Medicine, Kyung Hee University, Seoul 02447, Korea |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/31138996$$D View this record in MEDLINE/PubMed https://www.kci.go.kr/kciportal/ci/sereArticleSearch/ciSereArtiView.kci?sereArticleSearchBean.artiId=ART002464329$$DAccess content in National Research Foundation of Korea (NRF) |
| BookMark | eNqNUVtr2zAUNqNjzbq-72nocWM408WyrZdBSZut0G4hZM_iRDlutDqSK9kZ-SH9v1WW7gqDSXAOSN_lSN_z7Mh5h1n2ktGxLGn1Dt2YU6bGvB7zVNSTbMSpEnnNiuIoGzHOy5wn5HF2GuNXmpaUSrLyWXYsGBO1UuUouz_HFna4IouA0G_Q9cQ3ZAJdBGusI7PgV4PBSGYQegstufa9D2SOxm8x7MhyRy7cGlzC3pBz38HGOiTTwZneekeSwvVsRt6SvMWYDpLRHPpIthbIxLYWksQnHILvg-_W1pApmKT_InvaQBvx9LGfZF-mF4vJx_zq84fLydlVbgpB-5xXDHFl6qIuUdVCQslUTQumBFIhgJmGSdkUlKcNTAjOa6ioKpeVQamgEifZm4OuC42-NVZ7sN_7jde3QZ_NF5dailJWfI9lB-zgOth9g7bVXbCb9ALNqN4notHpfSKa15qnohLn_YHTDctNmjR9b4BfvL3bnzfOrpP3VpeSlymjJPD6USD4uwFjrzc2GmxbcOiHqDkXrJYVlUWCvvrd66fJj6wTgB4AJvgYAzb_M3_5F8XYHvbJpmlt-2_iA-AjztA |
| CitedBy_id | crossref_primary_10_3390_molecules27082484 crossref_primary_10_3389_fcell_2020_584513 crossref_primary_10_3390_ijms22168920 crossref_primary_10_4103_NRR_NRR_D_24_00172 crossref_primary_10_2174_0113892010277933231122111244 crossref_primary_10_1002_glia_24013 crossref_primary_10_22159_ajpcr_2022_v15i7_44405 crossref_primary_10_3390_ijms25010368 crossref_primary_10_3390_molecules29010181 crossref_primary_10_1016_j_brainres_2024_149414 crossref_primary_10_3389_fnagi_2020_587403 crossref_primary_10_5607_en21032 crossref_primary_10_2174_0929866529666220905105800 crossref_primary_10_3389_fphys_2022_814285 crossref_primary_10_3390_molecules29235700 |
| Cites_doi | 10.1167/iovs.08-3013 10.7150/ijms.18623 10.1007/s11064-017-2388-4 10.1089/10430340050015220 10.1126/science.1184334 10.1038/sj.gt.3301682 10.1523/JNEUROSCI.23-10-04127.2003 10.1038/emm.2016.159 10.1002/mds.23442 10.1038/srep14764 10.1126/scitranslmed.aaf1629 10.1016/S0006-8993(97)01100-1 10.1016/S0736-5748(03)00087-X 10.1006/mcne.2001.0985 10.1038/365027a0 10.1016/0306-4522(93)90491-W 10.1523/JNEUROSCI.23-13-05877.2003 10.1038/nature05957 10.1093/brain/awv297 10.1016/j.brainresbull.2012.07.001 10.1523/JNEUROSCI.0942-10.2010 10.1016/j.neuroscience.2018.01.052 10.1006/exnr.1996.0011 10.1016/S0006-8993(98)01244-X 10.1371/journal.pone.0121803 10.1126/science.2587985 10.1073/pnas.90.13.6315 10.1074/jbc.M116.762344 10.1016/j.bbi.2017.03.007 10.1007/BF00995382 10.1002/(SICI)1097-4547(19960201)43:3<331::AID-JNR7>3.0.CO;2-K 10.1111/jnc.12652 10.1111/j.1471-4159.2012.07712.x 10.1002/(SICI)1096-9861(19960101)364:1<68::AID-CNE6>3.0.CO;2-Q 10.3390/ijms19113543 10.1002/ar.1092310411 10.1038/342920a0 |
| ContentType | Journal Article |
| Copyright | Copyright © Experimental Neurobiology 2019. 2019 Experimental Neurobiology |
| Copyright_xml | – notice: Copyright © Experimental Neurobiology 2019. 2019 Experimental Neurobiology |
| DBID | AAYXX CITATION NPM 7X8 5PM ADTOC UNPAY ACYCR |
| DOI | 10.5607/en.2019.28.2.289 |
| DatabaseName | CrossRef PubMed MEDLINE - Academic PubMed Central (Full Participant titles) Unpaywall for CDI: Periodical Content Unpaywall Korean Citation Index |
| DatabaseTitle | CrossRef PubMed MEDLINE - Academic |
| DatabaseTitleList | PubMed MEDLINE - Academic |
| Database_xml | – sequence: 1 dbid: NPM name: PubMed url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database |
| DeliveryMethod | fulltext_linktorsrc |
| Discipline | Anatomy & Physiology |
| EISSN | 2093-8144 |
| EndPage | 299 |
| ExternalDocumentID | oai_kci_go_kr_ARTI_5365727 10.5607/en.2019.28.2.289 PMC6526113 31138996 10_5607_en_2019_28_2_289 |
| Genre | Journal Article |
| GrantInformation_xml | – fundername: ; grantid: 2018R1A6A1A03025124 – fundername: ; grantid: NRF-2016R1A2B4010692; NRF-2017M3C7A1031105; NRF-2016R1A6A3A11932765 |
| GroupedDBID | 5-W 8JR 8XY AAYXX ADBBV ALMA_UNASSIGNED_HOLDINGS AOIJS CITATION EF. HYE KQ8 M48 OK1 PGMZT RPM ADRAZ M~E NPM 7X8 5PM ADTOC UNPAY ACYCR |
| ID | FETCH-LOGICAL-c430t-271eedc8486e9835a619804193e033a1cf155f402020a133228a7096b7ce59a73 |
| IEDL.DBID | M48 |
| ISSN | 1226-2560 2093-8144 |
| IngestDate | Tue Nov 21 21:40:39 EST 2023 Wed Aug 20 00:10:52 EDT 2025 Tue Sep 30 16:46:12 EDT 2025 Fri Jul 11 09:54:07 EDT 2025 Thu Jan 02 23:01:42 EST 2025 Thu Apr 24 23:04:29 EDT 2025 Tue Jul 01 02:48:18 EDT 2025 |
| IsDoiOpenAccess | true |
| IsOpenAccess | true |
| IsPeerReviewed | true |
| IsScholarly | true |
| Issue | 2 |
| Keywords | Dopaminergic neuron Parkinson's disease Astrocyte TRPV1 Ciliary neurotrophic factor |
| Language | English |
| License | http://creativecommons.org/licenses/by-nc/4.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
| LinkModel | DirectLink |
| MergedId | FETCHMERGED-LOGICAL-c430t-271eedc8486e9835a619804193e033a1cf155f402020a133228a7096b7ce59a73 |
| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 These authors contributed equally to this work. |
| OpenAccessLink | http://journals.scholarsportal.info/openUrl.xqy?doi=10.5607/en.2019.28.2.289 |
| PMID | 31138996 |
| PQID | 2231857054 |
| PQPubID | 23479 |
| PageCount | 11 |
| ParticipantIDs | nrf_kci_oai_kci_go_kr_ARTI_5365727 unpaywall_primary_10_5607_en_2019_28_2_289 pubmedcentral_primary_oai_pubmedcentral_nih_gov_6526113 proquest_miscellaneous_2231857054 pubmed_primary_31138996 crossref_primary_10_5607_en_2019_28_2_289 crossref_citationtrail_10_5607_en_2019_28_2_289 |
| ProviderPackageCode | CITATION AAYXX |
| PublicationCentury | 2000 |
| PublicationDate | 2019-04-01 |
| PublicationDateYYYYMMDD | 2019-04-01 |
| PublicationDate_xml | – month: 04 year: 2019 text: 2019-04-01 day: 01 |
| PublicationDecade | 2010 |
| PublicationPlace | Korea (South) |
| PublicationPlace_xml | – name: Korea (South) |
| PublicationTitle | Experimental neurobiology |
| PublicationTitleAlternate | Exp Neurobiol |
| PublicationYear | 2019 |
| Publisher | The Korean Society for Brain and Neural Science 한국뇌신경과학회 |
| Publisher_xml | – name: The Korean Society for Brain and Neural Science – name: 한국뇌신경과학회 |
| References | West (10.5607/en.2019.28.2.289_ref23) 1991; 231 Won (10.5607/en.2019.28.2.289_ref2) 2016; 8 Chaturvedi (10.5607/en.2019.28.2.289_ref13) 2003; 21 Gerhardt (10.5607/en.2019.28.2.289_ref16) 1999; 817 Kells (10.5607/en.2019.28.2.289_ref17) 2010; 30 Bartus (10.5607/en.2019.28.2.289_ref21) 2011; 26 Nam (10.5607/en.2019.28.2.289_ref1) 2015; 138 Stöckli (10.5607/en.2019.28.2.289_ref36) 1989; 342 Park (10.5607/en.2019.28.2.289_ref5) 2012; 89 Lapchak (10.5607/en.2019.28.2.289_ref27) 1997; 777 Baek (10.5607/en.2019.28.2.289_ref34) 2018; 19 Yurek (10.5607/en.2019.28.2.289_ref15) 1996; 137 Jeong (10.5607/en.2019.28.2.289_ref8) 2015; 10 Lindholm (10.5607/en.2019.28.2.289_ref14) 2007; 448 Wang (10.5607/en.2019.28.2.289_ref28) 2002; 9 Jin (10.5607/en.2019.28.2.289_ref20) 1996; 43 Chung (10.5607/en.2019.28.2.289_ref3) 2017; 49 Huotarinen (10.5607/en.2019.28.2.289_ref30) 2018; 374 Shin (10.5607/en.2019.28.2.289_ref26) 2015; 5 Masu (10.5607/en.2019.28.2.289_ref9) 1993; 365 Salvatore (10.5607/en.2019.28.2.289_ref33) 2014; 129 Jorge-Finnigan (10.5607/en.2019.28.2.289_ref31) 2017; 292 Pease (10.5607/en.2019.28.2.289_ref11) 2009; 50 Mittoux (10.5607/en.2019.28.2.289_ref12) 2000; 11 Lee (10.5607/en.2019.28.2.289_ref24) 2010; 330 Lin (10.5607/en.2019.28.2.289_ref37) 1989; 246 Oyesiku (10.5607/en.2019.28.2.289_ref10) 1996; 364 Choi (10.5607/en.2019.28.2.289_ref22) 2003; 23 Paxinos (10.5607/en.2019.28.2.289_ref18) 2013 Kong (10.5607/en.2019.28.2.289_ref4) 2017; 64 Kamiguchi (10.5607/en.2019.28.2.289_ref38) 1995; 20 Shi (10.5607/en.2019.28.2.289_ref25) 2012; 121 Reiness (10.5607/en.2019.28.2.289_ref35) 2001; 17 Wang (10.5607/en.2019.28.2.289_ref29) 2017; 14 Zhao (10.5607/en.2019.28.2.289_ref6) 2017; 42 Herman (10.5607/en.2019.28.2.289_ref32) 1993; 53 Veldhuis (10.5607/en.2019.28.2.289_ref19) 2003; 23 Hagg (10.5607/en.2019.28.2.289_ref7) 1993; 90 |
| References_xml | – volume: 50 start-page: 2194 year: 2009 ident: 10.5607/en.2019.28.2.289_ref11 publication-title: Invest Ophthalmol Vis Sci doi: 10.1167/iovs.08-3013 – volume: 14 start-page: 340 year: 2017 ident: 10.5607/en.2019.28.2.289_ref29 publication-title: Int J Med Sci doi: 10.7150/ijms.18623 – volume: 42 start-page: 3431 year: 2017 ident: 10.5607/en.2019.28.2.289_ref6 publication-title: Neurochem Res doi: 10.1007/s11064-017-2388-4 – volume: 11 start-page: 1177 year: 2000 ident: 10.5607/en.2019.28.2.289_ref12 publication-title: Hum Gene Ther doi: 10.1089/10430340050015220 – volume: 330 start-page: 790 year: 2010 ident: 10.5607/en.2019.28.2.289_ref24 publication-title: Science doi: 10.1126/science.1184334 – volume: 9 start-page: 381 year: 2002 ident: 10.5607/en.2019.28.2.289_ref28 publication-title: Gene Ther doi: 10.1038/sj.gt.3301682 – volume: 23 start-page: 4127 year: 2003 ident: 10.5607/en.2019.28.2.289_ref19 publication-title: J Neurosci doi: 10.1523/JNEUROSCI.23-10-04127.2003 – volume: 49 start-page: e298 year: 2017 ident: 10.5607/en.2019.28.2.289_ref3 publication-title: Exp Mol Med doi: 10.1038/emm.2016.159 – volume: 26 start-page: 27 year: 2011 ident: 10.5607/en.2019.28.2.289_ref21 publication-title: Mov Disord doi: 10.1002/mds.23442 – volume: 5 start-page: 14764 year: 2015 ident: 10.5607/en.2019.28.2.289_ref26 publication-title: Sci Rep doi: 10.1038/srep14764 – volume: 8 start-page: 367ra170 year: 2016 ident: 10.5607/en.2019.28.2.289_ref2 publication-title: Sci Transl Med doi: 10.1126/scitranslmed.aaf1629 – volume: 777 start-page: 153 year: 1997 ident: 10.5607/en.2019.28.2.289_ref27 publication-title: Brain Res doi: 10.1016/S0006-8993(97)01100-1 – volume: 21 start-page: 391 year: 2003 ident: 10.5607/en.2019.28.2.289_ref13 publication-title: Int J Dev Neurosci doi: 10.1016/S0736-5748(03)00087-X – volume: 17 start-page: 931 year: 2001 ident: 10.5607/en.2019.28.2.289_ref35 publication-title: Mol Cell Neurosci doi: 10.1006/mcne.2001.0985 – volume: 365 start-page: 27 year: 1993 ident: 10.5607/en.2019.28.2.289_ref9 publication-title: Nature doi: 10.1038/365027a0 – volume: 53 start-page: 1083 year: 1993 ident: 10.5607/en.2019.28.2.289_ref32 publication-title: Neuroscience doi: 10.1016/0306-4522(93)90491-W – volume: 23 start-page: 5877 year: 2003 ident: 10.5607/en.2019.28.2.289_ref22 publication-title: J Neurosci doi: 10.1523/JNEUROSCI.23-13-05877.2003 – volume: 448 start-page: 73 year: 2007 ident: 10.5607/en.2019.28.2.289_ref14 publication-title: Nature doi: 10.1038/nature05957 – volume: 138 start-page: 3610 year: 2015 ident: 10.5607/en.2019.28.2.289_ref1 publication-title: Brain doi: 10.1093/brain/awv297 – volume: 89 start-page: 92 year: 2012 ident: 10.5607/en.2019.28.2.289_ref5 publication-title: Brain Res Bull doi: 10.1016/j.brainresbull.2012.07.001 – volume: 30 start-page: 9567 year: 2010 ident: 10.5607/en.2019.28.2.289_ref17 publication-title: J Neurosci doi: 10.1523/JNEUROSCI.0942-10.2010 – volume: 374 start-page: 250 year: 2018 ident: 10.5607/en.2019.28.2.289_ref30 publication-title: Neuroscience doi: 10.1016/j.neuroscience.2018.01.052 – volume: 137 start-page: 105 year: 1996 ident: 10.5607/en.2019.28.2.289_ref15 publication-title: Exp Neurol doi: 10.1006/exnr.1996.0011 – volume: 817 start-page: 163 year: 1999 ident: 10.5607/en.2019.28.2.289_ref16 publication-title: Brain Res doi: 10.1016/S0006-8993(98)01244-X – volume: 10 start-page: e0121803 year: 2015 ident: 10.5607/en.2019.28.2.289_ref8 publication-title: PLoS One doi: 10.1371/journal.pone.0121803 – volume: 246 start-page: 1023 year: 1989 ident: 10.5607/en.2019.28.2.289_ref37 publication-title: Science doi: 10.1126/science.2587985 – volume: 90 start-page: 6315 year: 1993 ident: 10.5607/en.2019.28.2.289_ref7 publication-title: Proc Natl Acad Sci U S A doi: 10.1073/pnas.90.13.6315 – volume: 292 start-page: 14092 year: 2017 ident: 10.5607/en.2019.28.2.289_ref31 publication-title: J Biol Chem doi: 10.1074/jbc.M116.762344 – volume: 64 start-page: 354 year: 2017 ident: 10.5607/en.2019.28.2.289_ref4 publication-title: Brain Behav Immun doi: 10.1016/j.bbi.2017.03.007 – volume: 20 start-page: 1187 year: 1995 ident: 10.5607/en.2019.28.2.289_ref38 publication-title: Neurochem Res doi: 10.1007/BF00995382 – volume: 43 start-page: 331 year: 1996 ident: 10.5607/en.2019.28.2.289_ref20 publication-title: J Neurosci Res doi: 10.1002/(SICI)1097-4547(19960201)43:3<331::AID-JNR7>3.0.CO;2-K – volume: 129 start-page: 548 year: 2014 ident: 10.5607/en.2019.28.2.289_ref33 publication-title: J Neurochem doi: 10.1111/jnc.12652 – volume-title: The rat brain in stereotaxic coordinates year: 2013 ident: 10.5607/en.2019.28.2.289_ref18 – volume: 121 start-page: 700 year: 2012 ident: 10.5607/en.2019.28.2.289_ref25 publication-title: J Neurochem doi: 10.1111/j.1471-4159.2012.07712.x – volume: 364 start-page: 68 year: 1996 ident: 10.5607/en.2019.28.2.289_ref10 publication-title: J Comp Neurol doi: 10.1002/(SICI)1096-9861(19960101)364:1<68::AID-CNE6>3.0.CO;2-Q – volume: 19 start-page: E3543 year: 2018 ident: 10.5607/en.2019.28.2.289_ref34 publication-title: Int J Mol Sci doi: 10.3390/ijms19113543 – volume: 231 start-page: 482 year: 1991 ident: 10.5607/en.2019.28.2.289_ref23 publication-title: Anat Rec doi: 10.1002/ar.1092310411 – volume: 342 start-page: 920 year: 1989 ident: 10.5607/en.2019.28.2.289_ref36 publication-title: Nature doi: 10.1038/342920a0 |
| SSID | ssj0000559516 |
| Score | 2.166553 |
| Snippet | Transient receptor potential vanilloid subtype 1 (TRPV1) on astrocytes prevents ongoing degeneration of nigrostriatal dopamine (DA) neurons in MPP
-lesioned... Transient receptor potential vanilloid subtype 1 (TRPV1) on astrocytes prevents ongoing degeneration of nigrostriatal dopamine (DA) neurons in MPP+-lesioned... |
| SourceID | nrf unpaywall pubmedcentral proquest pubmed crossref |
| SourceType | Open Website Open Access Repository Aggregation Database Index Database Enrichment Source |
| StartPage | 289 |
| SubjectTerms | Original 뇌과학 |
| Title | Delayed Treatment of Capsaicin Produces Partial Motor Recovery by Enhancing Dopamine Function in MPP + -lesioned Rats via Ciliary Neurotrophic Factor |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/31138996 https://www.proquest.com/docview/2231857054 https://pubmed.ncbi.nlm.nih.gov/PMC6526113 https://www.en-journal.org/journal/download_pdf.php?doi=10.5607/en.2019.28.2.289 https://www.kci.go.kr/kciportal/ci/sereArticleSearch/ciSereArtiView.kci?sereArticleSearchBean.artiId=ART002464329 |
| UnpaywallVersion | publishedVersion |
| Volume | 28 |
| hasFullText | 1 |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| ispartofPNX | Experimental Neurobiology, 2019, 28(2), , pp.289-299 |
| journalDatabaseRights | – providerCode: PRVAFT databaseName: Open Access Digital Library customDbUrl: eissn: 2093-8144 dateEnd: 99991231 omitProxy: true ssIdentifier: ssj0000559516 issn: 2093-8144 databaseCode: KQ8 dateStart: 20100101 isFulltext: true titleUrlDefault: http://grweb.coalliance.org/oadl/oadl.html providerName: Colorado Alliance of Research Libraries – providerCode: PRVERR databaseName: KoreaMed Open Access customDbUrl: eissn: 2093-8144 dateEnd: 99991231 omitProxy: true ssIdentifier: ssj0000559516 issn: 2093-8144 databaseCode: 5-W dateStart: 20080101 isFulltext: true titleUrlDefault: https://koreamed.org/journals providerName: Korean Association of Medical Journal Editors – providerCode: PRVAQN databaseName: PubMed Central customDbUrl: eissn: 2093-8144 dateEnd: 99991231 omitProxy: true ssIdentifier: ssj0000559516 issn: 2093-8144 databaseCode: RPM dateStart: 20100101 isFulltext: true titleUrlDefault: https://www.ncbi.nlm.nih.gov/pmc/ providerName: National Library of Medicine – providerCode: PRVFZP databaseName: Scholars Portal Journals: Open Access customDbUrl: eissn: 2093-8144 dateEnd: 20250831 omitProxy: true ssIdentifier: ssj0000559516 issn: 2093-8144 databaseCode: M48 dateStart: 20100601 isFulltext: true titleUrlDefault: http://journals.scholarsportal.info providerName: Scholars Portal |
| link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwjV1Nb9NAEF3RcoALAgrUfGlBCAmQU3vXnydUpY0KUlCEGqm31dheN1ZdO9gO4N_BH2bGdgIREXBxDrHX3sxM5j3P7hvGXukE_DBNQzOy49R03CjA_8EkNHXiBy41t7aAKrrTT97Z3Pl44V782h49_ID1TmpH_aTmVT76_qV9jwGP-HWE-do_0qRjaocjEYwEHsI9dhPzkiAfnw5gv1f6dhFOdNuNEHOYlOv7uuXOQbby1F5Rpbsg6J8rKW-tiiW03yDPf0tTk7vszoAv-XHvEPfYDV3cZwfHBXLr65a_5t2Kz-5V-gH7caJzaHXCz9erzXmZ8jEsa6B6O591arC65jPyLxx1WiJD58RYMQBaHrX8tFiQYEdxyU-QfV8jZOUTzJRkbY4jTGezd2auuyY-Cf8MTc2_ZsDHWZ4BDtApgzRVuVxkMZ90nX8esPnk9Hx8Zg5NGszYkVZjCt_GNBsHTuDpEOEcICMjTaNQaktKQA9AxJISSxUWICEWIgAfeVPk0wYw8OVDtl_gQxwyDprAGUQ6cABxoht4npbCSrVOPWlFYLCjtUlUPCiYUyONXCGTISNipCsyohKBEngIDfZmc8WyV-_4y7kv0crqKs4USW7T52WpriqFxOKDcqXnItQz2Iu1EyiMQyquQKHLVa0QZpGsFiJggz3qnWJzS2lTOTj0DOZvucvmBLrh9jdFtui0vj0XKa4tDfZ241j_nMnj_5nJE3abLuoXIT1l-0210s8QXzXR8y5sfgLR3yHS |
| linkProvider | Scholars Portal |
| openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Delayed+Treatment+of+Capsaicin+Produces+Partial+Motor+Recovery+by+Enhancing+Dopamine+Function+in+MPP%2B-lesioned+Rats+via+Ciliary+Neurotrophic+Factor&rft.jtitle=Experimental+neurobiology&rft.au=%EA%B9%80%EA%B2%BD%EC%9D%B8%28%EA%B2%BD%ED%9D%AC%EB%8C%80%ED%95%99%EA%B5%90+%EC%8B%A0%EA%B2%BD%ED%87%B4%ED%99%94%EC%A0%9C%EC%96%B4%EC%97%B0%EA%B5%AC%EC%86%8C&rft.au=%EB%B0%B1%EC%A0%95%EC%97%BD&rft.au=%EC%A0%95%EC%9E%AC%EC%98%81&rft.au=%EB%82%A8%EC%A7%84%ED%95%9C&rft.date=2019-04-01&rft.pub=%ED%95%9C%EA%B5%AD%EB%87%8C%EC%8B%A0%EA%B2%BD%EA%B3%BC%ED%95%99%ED%9A%8C&rft.issn=1226-2560&rft.eissn=2093-8144&rft.spage=289&rft.epage=299&rft_id=info:doi/10.5607%2Fen.2019.28.2.289&rft.externalDBID=n%2Fa&rft.externalDocID=oai_kci_go_kr_ARTI_5365727 |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1226-2560&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1226-2560&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1226-2560&client=summon |