Crocin Reverses Depression-Like Behavior in Parkinson Disease Mice via VTA-mPFC Pathway
Depression is a common non-motor symptom in patients with Parkinson’s disease (PD) and difficult to treat. Crocin is a natural multipotential neuroprotective compound that has been shown to elicit antidepressant activity and is promising for the therapy of neuropsychological diseases. Here, we inves...
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| Veröffentlicht in: | Molecular neurobiology 2020-07, Vol.57 (7), p.3158-3170 |
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| container_title | Molecular neurobiology |
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| creator | Tang, Juanjuan Lu, Linyu Wang, Qisheng Liu, Hou Xue, Wenda Zhou, Tong Xu, Liantiao Wang, Kai Wu, Die Wei, Fei Tao, Weiwei Chen, Gang |
| description | Depression is a common non-motor symptom in patients with Parkinson’s disease (PD) and difficult to treat. Crocin is a natural multipotential neuroprotective compound that has been shown to elicit antidepressant activity and is promising for the therapy of neuropsychological diseases. Here, we investigated the therapeutic effect of crocin in a mouse model of Parkinson’s disease depression (PDD) and clarified the underlying mechanism. We prepared 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced subacute mouse model of PD, and found that around 60% of the model mice showed depression-like behavior, using the forced swimming test (FST). A regime of 10-day treatment of crocin alleviated the PDD symptoms. The crocin reduced the structural damage in soma volume and axon length of neurons and inhibited their spontaneous discharge in dopaminergic (DA) neurons in the ventral tegmental area (VTA). Notably, the MPTP-treated mice showed the decrease in the critical signaling for synaptic plasticity, including the proteins of PSD-95, synapsin-1, and GluR-1, in the medial prefrontal cortex (mPFC) where it receives efferent from VTA and regulates depression-like behavior. However, crocin treatment rescued the defect of the mammalian target of rapamycin (mTOR) signaling in PDD mice. Furthermore, the antidepressant action of crocin was blunted after blockade of mTOR signaling with the antagonist rapamycin. In conclusion, our study demonstrated that crocin protected the DA projection neurons in the VTA through activating mTOR, which subsequently improved the neural synaptic plasticity of mPFC, and ameliorated depression-like behavior in PD mice. |
| doi_str_mv | 10.1007/s12035-020-01941-2 |
| format | Article |
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Crocin is a natural multipotential neuroprotective compound that has been shown to elicit antidepressant activity and is promising for the therapy of neuropsychological diseases. Here, we investigated the therapeutic effect of crocin in a mouse model of Parkinson’s disease depression (PDD) and clarified the underlying mechanism. We prepared 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced subacute mouse model of PD, and found that around 60% of the model mice showed depression-like behavior, using the forced swimming test (FST). A regime of 10-day treatment of crocin alleviated the PDD symptoms. The crocin reduced the structural damage in soma volume and axon length of neurons and inhibited their spontaneous discharge in dopaminergic (DA) neurons in the ventral tegmental area (VTA). Notably, the MPTP-treated mice showed the decrease in the critical signaling for synaptic plasticity, including the proteins of PSD-95, synapsin-1, and GluR-1, in the medial prefrontal cortex (mPFC) where it receives efferent from VTA and regulates depression-like behavior. However, crocin treatment rescued the defect of the mammalian target of rapamycin (mTOR) signaling in PDD mice. Furthermore, the antidepressant action of crocin was blunted after blockade of mTOR signaling with the antagonist rapamycin. In conclusion, our study demonstrated that crocin protected the DA projection neurons in the VTA through activating mTOR, which subsequently improved the neural synaptic plasticity of mPFC, and ameliorated depression-like behavior in PD mice.</description><identifier>ISSN: 0893-7648</identifier><identifier>EISSN: 1559-1182</identifier><identifier>DOI: 10.1007/s12035-020-01941-2</identifier><identifier>PMID: 32495180</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Animal models ; Animals ; Antidepressants ; Behavior, Animal - drug effects ; Biomedical and Life Sciences ; Biomedicine ; Carotenoids - pharmacology ; Cell Biology ; Depression - metabolism ; Dopamine receptors ; Glutamate receptors ; Male ; Mental depression ; Mice ; Movement disorders ; MPTP ; Neural Pathways - drug effects ; Neurobiology ; Neurodegenerative diseases ; Neurology ; Neuronal Plasticity - drug effects ; Neurons ; Neuroplasticity ; Neuroprotection ; Neurosciences ; Original Article ; Parkinson's disease ; Parkinsonian Disorders - metabolism ; Postsynaptic density proteins ; Prefrontal cortex ; Prefrontal Cortex - drug effects ; Prefrontal Cortex - metabolism ; Rapamycin ; Receptors, AMPA - metabolism ; Signal Transduction - drug effects ; Swimming behavior ; Synapsin ; Synapsins - metabolism ; Synaptic plasticity ; TOR protein ; Ventral Tegmental Area - drug effects ; Ventral Tegmental Area - metabolism ; Ventral tegmentum</subject><ispartof>Molecular neurobiology, 2020-07, Vol.57 (7), p.3158-3170</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature 2020</rights><rights>Springer Science+Business Media, LLC, part of Springer Nature 2020.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-1dd7dfc43e211b748a93c872b18227b3976739b0f5db40c28c2aab724d2042a03</citedby><cites>FETCH-LOGICAL-c375t-1dd7dfc43e211b748a93c872b18227b3976739b0f5db40c28c2aab724d2042a03</cites><orcidid>0000-0002-3507-1218</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12035-020-01941-2$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12035-020-01941-2$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27923,27924,41487,42556,51318</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32495180$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tang, Juanjuan</creatorcontrib><creatorcontrib>Lu, Linyu</creatorcontrib><creatorcontrib>Wang, Qisheng</creatorcontrib><creatorcontrib>Liu, Hou</creatorcontrib><creatorcontrib>Xue, Wenda</creatorcontrib><creatorcontrib>Zhou, Tong</creatorcontrib><creatorcontrib>Xu, Liantiao</creatorcontrib><creatorcontrib>Wang, Kai</creatorcontrib><creatorcontrib>Wu, Die</creatorcontrib><creatorcontrib>Wei, Fei</creatorcontrib><creatorcontrib>Tao, Weiwei</creatorcontrib><creatorcontrib>Chen, Gang</creatorcontrib><title>Crocin Reverses Depression-Like Behavior in Parkinson Disease Mice via VTA-mPFC Pathway</title><title>Molecular neurobiology</title><addtitle>Mol Neurobiol</addtitle><addtitle>Mol Neurobiol</addtitle><description>Depression is a common non-motor symptom in patients with Parkinson’s disease (PD) and difficult to treat. Crocin is a natural multipotential neuroprotective compound that has been shown to elicit antidepressant activity and is promising for the therapy of neuropsychological diseases. Here, we investigated the therapeutic effect of crocin in a mouse model of Parkinson’s disease depression (PDD) and clarified the underlying mechanism. We prepared 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced subacute mouse model of PD, and found that around 60% of the model mice showed depression-like behavior, using the forced swimming test (FST). A regime of 10-day treatment of crocin alleviated the PDD symptoms. The crocin reduced the structural damage in soma volume and axon length of neurons and inhibited their spontaneous discharge in dopaminergic (DA) neurons in the ventral tegmental area (VTA). Notably, the MPTP-treated mice showed the decrease in the critical signaling for synaptic plasticity, including the proteins of PSD-95, synapsin-1, and GluR-1, in the medial prefrontal cortex (mPFC) where it receives efferent from VTA and regulates depression-like behavior. However, crocin treatment rescued the defect of the mammalian target of rapamycin (mTOR) signaling in PDD mice. Furthermore, the antidepressant action of crocin was blunted after blockade of mTOR signaling with the antagonist rapamycin. In conclusion, our study demonstrated that crocin protected the DA projection neurons in the VTA through activating mTOR, which subsequently improved the neural synaptic plasticity of mPFC, and ameliorated depression-like behavior in PD mice.</description><subject>Animal models</subject><subject>Animals</subject><subject>Antidepressants</subject><subject>Behavior, Animal - drug effects</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Carotenoids - pharmacology</subject><subject>Cell Biology</subject><subject>Depression - metabolism</subject><subject>Dopamine receptors</subject><subject>Glutamate receptors</subject><subject>Male</subject><subject>Mental depression</subject><subject>Mice</subject><subject>Movement disorders</subject><subject>MPTP</subject><subject>Neural Pathways - drug effects</subject><subject>Neurobiology</subject><subject>Neurodegenerative diseases</subject><subject>Neurology</subject><subject>Neuronal Plasticity - drug effects</subject><subject>Neurons</subject><subject>Neuroplasticity</subject><subject>Neuroprotection</subject><subject>Neurosciences</subject><subject>Original Article</subject><subject>Parkinson's disease</subject><subject>Parkinsonian Disorders - metabolism</subject><subject>Postsynaptic density proteins</subject><subject>Prefrontal cortex</subject><subject>Prefrontal Cortex - drug effects</subject><subject>Prefrontal Cortex - metabolism</subject><subject>Rapamycin</subject><subject>Receptors, AMPA - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>Swimming behavior</subject><subject>Synapsin</subject><subject>Synapsins - metabolism</subject><subject>Synaptic plasticity</subject><subject>TOR protein</subject><subject>Ventral Tegmental Area - drug effects</subject><subject>Ventral Tegmental Area - metabolism</subject><subject>Ventral tegmentum</subject><issn>0893-7648</issn><issn>1559-1182</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</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>eNp9kE1vEzEQhi1ERdPCH-CAVuLCxXQ89sbrY0kpIKWiQv04Wl7vhLpNdlNPkqr_vqZpQeLQ0xzmmXdmHiHeK_isAOwBKwRdS0CQoJxREl-JkaprJ5Vq8LUYQeO0tGPT7Io95msARAX2jdjVaFytGhiJy0keYuqrX7ShzMTVES0zMaehl9N0Q9UXugqbNOSqQKch36Seh746SkyBqTpJkapNCtXF2aFcnB5PCrO6ugv3b8XOLMyZ3j3VfXF-_PVs8l1Of377MTmcyqhtvZKq62w3i0YTKtVa0wSnY2OxLQ-gbbWzY6tdC7O6aw1EbCKG0Fo0HYLBAHpffNrmLvNwuyZe-UXiSPN56GlYs0cDbmysgaagH_9Dr4d17st1hVJ27JxTtlC4pWIemDPN_DKnRcj3XoH_o91vtfui3T9q91iGPjxFr9sFdX9Hnj0XQG8BLq3-N-V_u1-IfQA2lYrW</recordid><startdate>20200701</startdate><enddate>20200701</enddate><creator>Tang, Juanjuan</creator><creator>Lu, Linyu</creator><creator>Wang, Qisheng</creator><creator>Liu, Hou</creator><creator>Xue, Wenda</creator><creator>Zhou, Tong</creator><creator>Xu, Liantiao</creator><creator>Wang, Kai</creator><creator>Wu, Die</creator><creator>Wei, Fei</creator><creator>Tao, Weiwei</creator><creator>Chen, Gang</creator><general>Springer US</general><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>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88G</scope><scope>88I</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>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>M2M</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-3507-1218</orcidid></search><sort><creationdate>20200701</creationdate><title>Crocin Reverses Depression-Like Behavior in Parkinson Disease Mice via VTA-mPFC Pathway</title><author>Tang, Juanjuan ; Lu, Linyu ; Wang, Qisheng ; Liu, Hou ; Xue, Wenda ; Zhou, Tong ; Xu, Liantiao ; Wang, Kai ; Wu, Die ; Wei, Fei ; Tao, Weiwei ; Chen, Gang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-1dd7dfc43e211b748a93c872b18227b3976739b0f5db40c28c2aab724d2042a03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Animal models</topic><topic>Animals</topic><topic>Antidepressants</topic><topic>Behavior, Animal - drug effects</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Carotenoids - pharmacology</topic><topic>Cell Biology</topic><topic>Depression - metabolism</topic><topic>Dopamine receptors</topic><topic>Glutamate receptors</topic><topic>Male</topic><topic>Mental depression</topic><topic>Mice</topic><topic>Movement disorders</topic><topic>MPTP</topic><topic>Neural Pathways - drug effects</topic><topic>Neurobiology</topic><topic>Neurodegenerative diseases</topic><topic>Neurology</topic><topic>Neuronal Plasticity - drug effects</topic><topic>Neurons</topic><topic>Neuroplasticity</topic><topic>Neuroprotection</topic><topic>Neurosciences</topic><topic>Original Article</topic><topic>Parkinson's disease</topic><topic>Parkinsonian Disorders - metabolism</topic><topic>Postsynaptic density proteins</topic><topic>Prefrontal cortex</topic><topic>Prefrontal Cortex - drug effects</topic><topic>Prefrontal Cortex - metabolism</topic><topic>Rapamycin</topic><topic>Receptors, AMPA - 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Academic</collection><jtitle>Molecular neurobiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tang, Juanjuan</au><au>Lu, Linyu</au><au>Wang, Qisheng</au><au>Liu, Hou</au><au>Xue, Wenda</au><au>Zhou, Tong</au><au>Xu, Liantiao</au><au>Wang, Kai</au><au>Wu, Die</au><au>Wei, Fei</au><au>Tao, Weiwei</au><au>Chen, Gang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Crocin Reverses Depression-Like Behavior in Parkinson Disease Mice via VTA-mPFC Pathway</atitle><jtitle>Molecular neurobiology</jtitle><stitle>Mol Neurobiol</stitle><addtitle>Mol Neurobiol</addtitle><date>2020-07-01</date><risdate>2020</risdate><volume>57</volume><issue>7</issue><spage>3158</spage><epage>3170</epage><pages>3158-3170</pages><issn>0893-7648</issn><eissn>1559-1182</eissn><abstract>Depression is a common non-motor symptom in patients with Parkinson’s disease (PD) and difficult to treat. Crocin is a natural multipotential neuroprotective compound that has been shown to elicit antidepressant activity and is promising for the therapy of neuropsychological diseases. Here, we investigated the therapeutic effect of crocin in a mouse model of Parkinson’s disease depression (PDD) and clarified the underlying mechanism. We prepared 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced subacute mouse model of PD, and found that around 60% of the model mice showed depression-like behavior, using the forced swimming test (FST). A regime of 10-day treatment of crocin alleviated the PDD symptoms. The crocin reduced the structural damage in soma volume and axon length of neurons and inhibited their spontaneous discharge in dopaminergic (DA) neurons in the ventral tegmental area (VTA). Notably, the MPTP-treated mice showed the decrease in the critical signaling for synaptic plasticity, including the proteins of PSD-95, synapsin-1, and GluR-1, in the medial prefrontal cortex (mPFC) where it receives efferent from VTA and regulates depression-like behavior. However, crocin treatment rescued the defect of the mammalian target of rapamycin (mTOR) signaling in PDD mice. Furthermore, the antidepressant action of crocin was blunted after blockade of mTOR signaling with the antagonist rapamycin. In conclusion, our study demonstrated that crocin protected the DA projection neurons in the VTA through activating mTOR, which subsequently improved the neural synaptic plasticity of mPFC, and ameliorated depression-like behavior in PD mice.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>32495180</pmid><doi>10.1007/s12035-020-01941-2</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0002-3507-1218</orcidid></addata></record> |
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| subjects | Animal models Animals Antidepressants Behavior, Animal - drug effects Biomedical and Life Sciences Biomedicine Carotenoids - pharmacology Cell Biology Depression - metabolism Dopamine receptors Glutamate receptors Male Mental depression Mice Movement disorders MPTP Neural Pathways - drug effects Neurobiology Neurodegenerative diseases Neurology Neuronal Plasticity - drug effects Neurons Neuroplasticity Neuroprotection Neurosciences Original Article Parkinson's disease Parkinsonian Disorders - metabolism Postsynaptic density proteins Prefrontal cortex Prefrontal Cortex - drug effects Prefrontal Cortex - metabolism Rapamycin Receptors, AMPA - metabolism Signal Transduction - drug effects Swimming behavior Synapsin Synapsins - metabolism Synaptic plasticity TOR protein Ventral Tegmental Area - drug effects Ventral Tegmental Area - metabolism Ventral tegmentum |
| title | Crocin Reverses Depression-Like Behavior in Parkinson Disease Mice via VTA-mPFC Pathway |
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