Calcitriol protection against dopamine loss induced by intracerebroventricular administration of 6-hydroxydopamine
Calcitriol has been implicated as an agent that has neuroprotective effects in various animal models of diseases, possibly by upregulating glial cell line-derived neurotrophic factor (GDNF). The present study examined the neuroprotective effects of calcitriol in a model of early Parkinson's dis...
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| Veröffentlicht in: | Neurochemical research 2006-04, Vol.31 (4), p.533-539 |
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| creator | Smith, Michael P Fletcher-Turner, Anita Yurek, David M Cass, Wayne A |
| description | Calcitriol has been implicated as an agent that has neuroprotective effects in various animal models of diseases, possibly by upregulating glial cell line-derived neurotrophic factor (GDNF). The present study examined the neuroprotective effects of calcitriol in a model of early Parkinson's disease. Rats were treated daily with calcitriol or saline for 7 days before an intraventricular injection of 6-hydroxydopamine (6-OHDA), and then for 1 day or daily for 3(1/2) to 4 weeks after lesioning. Evoked overflow and tissue content of dopamine (DA) were determined 3(1/2) to 4 weeks post lesion. The 8-day calcitriol treatment did not attenuate 6-OHDA-induced decreases in evoked overflow of DA, nor did it protect against 6-OHDA-induced reductions in tissue levels of DA in the striatum or substantia nigra. However, the long-term calcitriol treatment did significantly increase evoked overflow of DA, as well as the amount of DA in the striatum, compared to saline treated animals. GDNF was significantly increased in the substantia nigra, but not in the striatum, of non-lesioned, calcitriol treated rats. These results suggest that long-term treatment with calcitriol can provide partial protection for dopaminergic neurons against the effects of intraventricularly administered 6-OHDA. |
| doi_str_mv | 10.1007/s11064-006-9048-4 |
| format | Article |
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The present study examined the neuroprotective effects of calcitriol in a model of early Parkinson's disease. Rats were treated daily with calcitriol or saline for 7 days before an intraventricular injection of 6-hydroxydopamine (6-OHDA), and then for 1 day or daily for 3(1/2) to 4 weeks after lesioning. Evoked overflow and tissue content of dopamine (DA) were determined 3(1/2) to 4 weeks post lesion. The 8-day calcitriol treatment did not attenuate 6-OHDA-induced decreases in evoked overflow of DA, nor did it protect against 6-OHDA-induced reductions in tissue levels of DA in the striatum or substantia nigra. However, the long-term calcitriol treatment did significantly increase evoked overflow of DA, as well as the amount of DA in the striatum, compared to saline treated animals. GDNF was significantly increased in the substantia nigra, but not in the striatum, of non-lesioned, calcitriol treated rats. These results suggest that long-term treatment with calcitriol can provide partial protection for dopaminergic neurons against the effects of intraventricularly administered 6-OHDA.</description><identifier>ISSN: 0364-3190</identifier><identifier>EISSN: 1573-6903</identifier><identifier>DOI: 10.1007/s11064-006-9048-4</identifier><identifier>PMID: 16758362</identifier><language>eng</language><publisher>United States: Springer Nature B.V</publisher><subject>Animals ; Brain - anatomy & histology ; Brain - drug effects ; Brain - metabolism ; Brain-Derived Neurotrophic Factor - metabolism ; Calcitriol - pharmacology ; Disease Models, Animal ; Dopamine - metabolism ; Glial Cell Line-Derived Neurotrophic Factor - metabolism ; Male ; Microdialysis ; Neuroprotective Agents - pharmacology ; Oxidopamine - administration & dosage ; Oxidopamine - metabolism ; Parkinson Disease - metabolism ; Parkinson Disease - pathology ; Rats ; Rats, Inbred F344 ; Rats, Sprague-Dawley</subject><ispartof>Neurochemical research, 2006-04, Vol.31 (4), p.533-539</ispartof><rights>Springer Science+Business Media, Inc. 2006</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c357t-6b905ec943cb321acaf85c55fe5c6ea64ccfa7658630b8b16fd68dba59886c3</citedby><cites>FETCH-LOGICAL-c357t-6b905ec943cb321acaf85c55fe5c6ea64ccfa7658630b8b16fd68dba59886c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,778,782,27911,27912</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16758362$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Smith, Michael P</creatorcontrib><creatorcontrib>Fletcher-Turner, Anita</creatorcontrib><creatorcontrib>Yurek, David M</creatorcontrib><creatorcontrib>Cass, Wayne A</creatorcontrib><title>Calcitriol protection against dopamine loss induced by intracerebroventricular administration of 6-hydroxydopamine</title><title>Neurochemical research</title><addtitle>Neurochem Res</addtitle><description>Calcitriol has been implicated as an agent that has neuroprotective effects in various animal models of diseases, possibly by upregulating glial cell line-derived neurotrophic factor (GDNF). 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These results suggest that long-term treatment with calcitriol can provide partial protection for dopaminergic neurons against the effects of intraventricularly administered 6-OHDA.</description><subject>Animals</subject><subject>Brain - anatomy & histology</subject><subject>Brain - drug effects</subject><subject>Brain - metabolism</subject><subject>Brain-Derived Neurotrophic Factor - metabolism</subject><subject>Calcitriol - pharmacology</subject><subject>Disease Models, Animal</subject><subject>Dopamine - metabolism</subject><subject>Glial Cell Line-Derived Neurotrophic Factor - metabolism</subject><subject>Male</subject><subject>Microdialysis</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>Oxidopamine - administration & dosage</subject><subject>Oxidopamine - metabolism</subject><subject>Parkinson Disease - metabolism</subject><subject>Parkinson Disease - pathology</subject><subject>Rats</subject><subject>Rats, Inbred F344</subject><subject>Rats, Sprague-Dawley</subject><issn>0364-3190</issn><issn>1573-6903</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqFkc1KxDAURoMozjj6AG6kuHBXvWmS23Qpg38guNB9SNNUM3SaMWnFeXszzojgxlUS7vk-uDmEnFK4pADlVaQUkOcAmFfAZc73yJSKkuVYAdsnU2BpymgFE3IU4wIgpQp6SCYUSyEZFlMS5rozbgjOd9kq-MGawfk-06_a9XHIGr_SS9fbrPMxZq5vRmObrF6n6xC0scHWwX_Y9HBm7HTIdJNwF9Pwu8e3GeZv6yb4z_VP1zE5aHUX7cnunJHn25uX-X3--HT3ML9-zA0T5ZBjXYGwpuLM1Kyg2uhWCiNEa4VBq5Eb0-oShUQGtawptg3KptaikhINm5GLbWva6n20cVBLF43tOt1bP0aFEgQvOPwL0opViMASeP4HXPgx9GkFVRS0RF4CTRDdQiakHwu2VavgljqsFQW1kaa20lSSpjbSFE-Zs13xWC9t85vYWWJfbGyVTg</recordid><startdate>200604</startdate><enddate>200604</enddate><creator>Smith, Michael P</creator><creator>Fletcher-Turner, Anita</creator><creator>Yurek, David M</creator><creator>Cass, Wayne A</creator><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QR</scope><scope>7TK</scope><scope>7U7</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>200604</creationdate><title>Calcitriol protection against dopamine loss induced by intracerebroventricular administration of 6-hydroxydopamine</title><author>Smith, Michael P ; 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The present study examined the neuroprotective effects of calcitriol in a model of early Parkinson's disease. Rats were treated daily with calcitriol or saline for 7 days before an intraventricular injection of 6-hydroxydopamine (6-OHDA), and then for 1 day or daily for 3(1/2) to 4 weeks after lesioning. Evoked overflow and tissue content of dopamine (DA) were determined 3(1/2) to 4 weeks post lesion. The 8-day calcitriol treatment did not attenuate 6-OHDA-induced decreases in evoked overflow of DA, nor did it protect against 6-OHDA-induced reductions in tissue levels of DA in the striatum or substantia nigra. However, the long-term calcitriol treatment did significantly increase evoked overflow of DA, as well as the amount of DA in the striatum, compared to saline treated animals. GDNF was significantly increased in the substantia nigra, but not in the striatum, of non-lesioned, calcitriol treated rats. These results suggest that long-term treatment with calcitriol can provide partial protection for dopaminergic neurons against the effects of intraventricularly administered 6-OHDA.</abstract><cop>United States</cop><pub>Springer Nature B.V</pub><pmid>16758362</pmid><doi>10.1007/s11064-006-9048-4</doi><tpages>7</tpages></addata></record> |
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| ispartof | Neurochemical research, 2006-04, Vol.31 (4), p.533-539 |
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| subjects | Animals Brain - anatomy & histology Brain - drug effects Brain - metabolism Brain-Derived Neurotrophic Factor - metabolism Calcitriol - pharmacology Disease Models, Animal Dopamine - metabolism Glial Cell Line-Derived Neurotrophic Factor - metabolism Male Microdialysis Neuroprotective Agents - pharmacology Oxidopamine - administration & dosage Oxidopamine - metabolism Parkinson Disease - metabolism Parkinson Disease - pathology Rats Rats, Inbred F344 Rats, Sprague-Dawley |
| title | Calcitriol protection against dopamine loss induced by intracerebroventricular administration of 6-hydroxydopamine |
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