Differential ultrastructural alterations in the Vglut2 glutamatergic input to the substantia nigra pars compacta/pars reticulata following nigrostriatal dopamine loss in a progressive mouse model of Parkinson’s disease
Loss of nigrostriatal dopamine (DA) in Parkinson's disease results in over‐activation/bursting of the subthalamic nucleus (STN). The STN projects to the substantia nigra (SN) pars compacta (SNpc) and pars reticulata (SNpr). The vesicular glutamate transporter 2 (Vglut2) is localized within at l...
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| Veröffentlicht in: | The European journal of neuroscience 2021-04, Vol.53 (7), p.2061-2077 |
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| creator | Moore, Cynthia Xu, Mo Bohlen, Jerry K. Meshul, Charles K. |
| description | Loss of nigrostriatal dopamine (DA) in Parkinson's disease results in over‐activation/bursting of the subthalamic nucleus (STN). The STN projects to the substantia nigra (SN) pars compacta (SNpc) and pars reticulata (SNpr). The vesicular glutamate transporter 2 (Vglut2) is localized within at least STN terminals synapsing within the SN, but it is not known if there are differential changes in the Vglut2+ input to the SNpc versus SNpr following DA loss. The goal/rationale of this current study was to determine whether there were differential changes in the density/levels of glutamate immuno‐gold labeling within Vglut2+ nerve terminals synapsing in the SNpc/SNpr and in the proportion of Vglut2+ terminals contacting tyrosine hydroxylase (TH) positively(+) or negatively(−) labeled dendrites following DA loss. Within the SNpc, there was a significant increase (51.3%) in the density of nerve terminal glutamate immuno‐gold labeling within Vglut2+ terminals synapsing on TH(−) dendrites following MPTP versus the vehicle (VEH) group. There was a significant decrease (16%) in the percentage of Vglut2+ terminals contacting TH(+) labeled dendrites in the MPTP‐ versus VEH‐treated group within the SNpc. Within the SNpr, there was a significant decrease in the density of glutamate immuno‐gold labeling in Vglut2+ terminals contacting TH(+) (71.5%) and TH(−) (55.5%) labeled dendrites, suggesting an increase in glutamate release. There was no change in the percentage of Vglut2+ terminals contacting TH(+) or TH(−) dendrites in the SNpr. We conclude that there is a differential effect following DA loss on the glutamate input from Vglut2+ terminals synapsing within the SNpr versus SNpc.
The subthalamic nucleus (STN) sends Vglut2(+) (vesicular glutamate transporter 2)/glutamatergic axonal projections to at least the substantia nigra pars reticulata (SNpr), synapsing on both TH(−) negative (A,A1) and TH(+) positive (C,C1) labeled dendrites. Following dopamine loss, there is a decrease in the density of glutamate immuno‐gold labeling within Vglut2(+) nerve terminals synapsing on both TH(−)(B) and TH(+)(D) dendrites in the SNpr, suggesting increased glutamate release from the STN. |
| doi_str_mv | 10.1111/ejn.14894 |
| format | Article |
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The subthalamic nucleus (STN) sends Vglut2(+) (vesicular glutamate transporter 2)/glutamatergic axonal projections to at least the substantia nigra pars reticulata (SNpr), synapsing on both TH(−) negative (A,A1) and TH(+) positive (C,C1) labeled dendrites. Following dopamine loss, there is a decrease in the density of glutamate immuno‐gold labeling within Vglut2(+) nerve terminals synapsing on both TH(−)(B) and TH(+)(D) dendrites in the SNpr, suggesting increased glutamate release from the STN.</description><identifier>ISSN: 0953-816X</identifier><identifier>EISSN: 1460-9568</identifier><identifier>DOI: 10.1111/ejn.14894</identifier><identifier>PMID: 32619030</identifier><language>eng</language><publisher>France: Wiley Subscription Services, Inc</publisher><subject>Dendrites ; Dopamine ; Electrical stimuli ; electron microscopy ; Glutamatergic transmission ; Glutamic acid transporter ; Hydroxylase ; immunohistochemistry ; Labeling ; Movement disorders ; MPTP ; Nerve endings ; Neurodegenerative diseases ; Parkinson's disease ; Solitary tract nucleus ; Substantia nigra ; Subthalamic nucleus ; Tyrosine 3-monooxygenase ; vesicular glutamate transporter 2</subject><ispartof>The European journal of neuroscience, 2021-04, Vol.53 (7), p.2061-2077</ispartof><rights>Published 2020. This article is a U.S. Government work and is in the public domain in the USA.</rights><rights>Copyright © 2021 Federation of European Neuroscience Societies and John Wiley & Sons Ltd</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3534-e043b79a0b0bae784abe5b096148e6e436c972cd3f9a5d970259da2d7c1370c33</citedby><cites>FETCH-LOGICAL-c3534-e043b79a0b0bae784abe5b096148e6e436c972cd3f9a5d970259da2d7c1370c33</cites><orcidid>0000-0002-9852-8748</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fejn.14894$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fejn.14894$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32619030$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Moore, Cynthia</creatorcontrib><creatorcontrib>Xu, Mo</creatorcontrib><creatorcontrib>Bohlen, Jerry K.</creatorcontrib><creatorcontrib>Meshul, Charles K.</creatorcontrib><title>Differential ultrastructural alterations in the Vglut2 glutamatergic input to the substantia nigra pars compacta/pars reticulata following nigrostriatal dopamine loss in a progressive mouse model of Parkinson’s disease</title><title>The European journal of neuroscience</title><addtitle>Eur J Neurosci</addtitle><description>Loss of nigrostriatal dopamine (DA) in Parkinson's disease results in over‐activation/bursting of the subthalamic nucleus (STN). The STN projects to the substantia nigra (SN) pars compacta (SNpc) and pars reticulata (SNpr). The vesicular glutamate transporter 2 (Vglut2) is localized within at least STN terminals synapsing within the SN, but it is not known if there are differential changes in the Vglut2+ input to the SNpc versus SNpr following DA loss. The goal/rationale of this current study was to determine whether there were differential changes in the density/levels of glutamate immuno‐gold labeling within Vglut2+ nerve terminals synapsing in the SNpc/SNpr and in the proportion of Vglut2+ terminals contacting tyrosine hydroxylase (TH) positively(+) or negatively(−) labeled dendrites following DA loss. Within the SNpc, there was a significant increase (51.3%) in the density of nerve terminal glutamate immuno‐gold labeling within Vglut2+ terminals synapsing on TH(−) dendrites following MPTP versus the vehicle (VEH) group. There was a significant decrease (16%) in the percentage of Vglut2+ terminals contacting TH(+) labeled dendrites in the MPTP‐ versus VEH‐treated group within the SNpc. Within the SNpr, there was a significant decrease in the density of glutamate immuno‐gold labeling in Vglut2+ terminals contacting TH(+) (71.5%) and TH(−) (55.5%) labeled dendrites, suggesting an increase in glutamate release. There was no change in the percentage of Vglut2+ terminals contacting TH(+) or TH(−) dendrites in the SNpr. We conclude that there is a differential effect following DA loss on the glutamate input from Vglut2+ terminals synapsing within the SNpr versus SNpc.
The subthalamic nucleus (STN) sends Vglut2(+) (vesicular glutamate transporter 2)/glutamatergic axonal projections to at least the substantia nigra pars reticulata (SNpr), synapsing on both TH(−) negative (A,A1) and TH(+) positive (C,C1) labeled dendrites. Following dopamine loss, there is a decrease in the density of glutamate immuno‐gold labeling within Vglut2(+) nerve terminals synapsing on both TH(−)(B) and TH(+)(D) dendrites in the SNpr, suggesting increased glutamate release from the STN.</description><subject>Dendrites</subject><subject>Dopamine</subject><subject>Electrical stimuli</subject><subject>electron microscopy</subject><subject>Glutamatergic transmission</subject><subject>Glutamic acid transporter</subject><subject>Hydroxylase</subject><subject>immunohistochemistry</subject><subject>Labeling</subject><subject>Movement disorders</subject><subject>MPTP</subject><subject>Nerve endings</subject><subject>Neurodegenerative diseases</subject><subject>Parkinson's disease</subject><subject>Solitary tract nucleus</subject><subject>Substantia nigra</subject><subject>Subthalamic nucleus</subject><subject>Tyrosine 3-monooxygenase</subject><subject>vesicular glutamate transporter 2</subject><issn>0953-816X</issn><issn>1460-9568</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><recordid>eNp1kctu1TAQhiMEoqeFBS-ALLGhi_TYcZzLEpVyUwUsALGLJs4k-ODYqS9U3fEavBsrngSfnMICCS_GmplP_4zmz7JHjJ6x9La4M2esbNryTrZhZUXzVlTN3WxDW8HzhlWfj7Jj73eU0qYqxf3siBcVaymnm-znczWO6NAEBZpEHRz44KIM0aUcdEAHQVnjiTIkfEHyadIxFGQfYYbUnpRMvSUGEuxK-Nj7AHtBYtTkgCzgPJF2XkAG2K6Zw6Bk1BCAjFZre63MtNI2TVeprMlgF5iVQaKtX6cnIWcnh96rb0hmG_0-DqiJHcl7cF-V8db8-v7Dk0F5BI8PsnsjaI8Pb_-T7OOLiw_nr_LLdy9fnz-7zCUXvMyRlryvW6A97QHrpoQeRU_bKt0UKyx5Jdu6kAMfWxBDW9NCtAMUQy0Zr6nk_CR7etBNC15F9KGblZeoNRhMa3ZFWVAmBKvqhD75B93Z6EzarisEKzmvRNEk6vRAyXQQ73DsFqdmcDcdo93e8i5Z3q2WJ_bxrWLsZxz-kn88TsD2AFwrjTf_V-ou3rw9SP4G1v69VQ</recordid><startdate>202104</startdate><enddate>202104</enddate><creator>Moore, Cynthia</creator><creator>Xu, Mo</creator><creator>Bohlen, Jerry K.</creator><creator>Meshul, Charles K.</creator><general>Wiley Subscription Services, Inc</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-9852-8748</orcidid></search><sort><creationdate>202104</creationdate><title>Differential ultrastructural alterations in the Vglut2 glutamatergic input to the substantia nigra pars compacta/pars reticulata following nigrostriatal dopamine loss in a progressive mouse model of Parkinson’s disease</title><author>Moore, Cynthia ; Xu, Mo ; Bohlen, Jerry K. ; Meshul, Charles K.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3534-e043b79a0b0bae784abe5b096148e6e436c972cd3f9a5d970259da2d7c1370c33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Dendrites</topic><topic>Dopamine</topic><topic>Electrical stimuli</topic><topic>electron microscopy</topic><topic>Glutamatergic transmission</topic><topic>Glutamic acid transporter</topic><topic>Hydroxylase</topic><topic>immunohistochemistry</topic><topic>Labeling</topic><topic>Movement disorders</topic><topic>MPTP</topic><topic>Nerve endings</topic><topic>Neurodegenerative diseases</topic><topic>Parkinson's disease</topic><topic>Solitary tract nucleus</topic><topic>Substantia nigra</topic><topic>Subthalamic nucleus</topic><topic>Tyrosine 3-monooxygenase</topic><topic>vesicular glutamate transporter 2</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Moore, Cynthia</creatorcontrib><creatorcontrib>Xu, Mo</creatorcontrib><creatorcontrib>Bohlen, Jerry K.</creatorcontrib><creatorcontrib>Meshul, Charles K.</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>The European journal of neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Moore, Cynthia</au><au>Xu, Mo</au><au>Bohlen, Jerry K.</au><au>Meshul, Charles K.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Differential ultrastructural alterations in the Vglut2 glutamatergic input to the substantia nigra pars compacta/pars reticulata following nigrostriatal dopamine loss in a progressive mouse model of Parkinson’s disease</atitle><jtitle>The European journal of neuroscience</jtitle><addtitle>Eur J Neurosci</addtitle><date>2021-04</date><risdate>2021</risdate><volume>53</volume><issue>7</issue><spage>2061</spage><epage>2077</epage><pages>2061-2077</pages><issn>0953-816X</issn><eissn>1460-9568</eissn><abstract>Loss of nigrostriatal dopamine (DA) in Parkinson's disease results in over‐activation/bursting of the subthalamic nucleus (STN). The STN projects to the substantia nigra (SN) pars compacta (SNpc) and pars reticulata (SNpr). The vesicular glutamate transporter 2 (Vglut2) is localized within at least STN terminals synapsing within the SN, but it is not known if there are differential changes in the Vglut2+ input to the SNpc versus SNpr following DA loss. The goal/rationale of this current study was to determine whether there were differential changes in the density/levels of glutamate immuno‐gold labeling within Vglut2+ nerve terminals synapsing in the SNpc/SNpr and in the proportion of Vglut2+ terminals contacting tyrosine hydroxylase (TH) positively(+) or negatively(−) labeled dendrites following DA loss. Within the SNpc, there was a significant increase (51.3%) in the density of nerve terminal glutamate immuno‐gold labeling within Vglut2+ terminals synapsing on TH(−) dendrites following MPTP versus the vehicle (VEH) group. There was a significant decrease (16%) in the percentage of Vglut2+ terminals contacting TH(+) labeled dendrites in the MPTP‐ versus VEH‐treated group within the SNpc. Within the SNpr, there was a significant decrease in the density of glutamate immuno‐gold labeling in Vglut2+ terminals contacting TH(+) (71.5%) and TH(−) (55.5%) labeled dendrites, suggesting an increase in glutamate release. There was no change in the percentage of Vglut2+ terminals contacting TH(+) or TH(−) dendrites in the SNpr. We conclude that there is a differential effect following DA loss on the glutamate input from Vglut2+ terminals synapsing within the SNpr versus SNpc.
The subthalamic nucleus (STN) sends Vglut2(+) (vesicular glutamate transporter 2)/glutamatergic axonal projections to at least the substantia nigra pars reticulata (SNpr), synapsing on both TH(−) negative (A,A1) and TH(+) positive (C,C1) labeled dendrites. Following dopamine loss, there is a decrease in the density of glutamate immuno‐gold labeling within Vglut2(+) nerve terminals synapsing on both TH(−)(B) and TH(+)(D) dendrites in the SNpr, suggesting increased glutamate release from the STN.</abstract><cop>France</cop><pub>Wiley Subscription Services, Inc</pub><pmid>32619030</pmid><doi>10.1111/ejn.14894</doi><tpages>17</tpages><orcidid>https://orcid.org/0000-0002-9852-8748</orcidid></addata></record> |
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| subjects | Dendrites Dopamine Electrical stimuli electron microscopy Glutamatergic transmission Glutamic acid transporter Hydroxylase immunohistochemistry Labeling Movement disorders MPTP Nerve endings Neurodegenerative diseases Parkinson's disease Solitary tract nucleus Substantia nigra Subthalamic nucleus Tyrosine 3-monooxygenase vesicular glutamate transporter 2 |
| title | Differential ultrastructural alterations in the Vglut2 glutamatergic input to the substantia nigra pars compacta/pars reticulata following nigrostriatal dopamine loss in a progressive mouse model of Parkinson’s disease |
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