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Here we explored whether cocaine‐primed reinstatement was associated with increased activity of the gelatinases, MMP‐2 or MMP‐9, in the medial prefrontal cortex (mPFC) or dorsal hippocampus. Male Sprague‐Dawley rats underwent training for cocaine‐CPP followed by extinction sessions and either saline‐ or cocaine‐priming injections. Cocaine‐induced reinstatement produced significant increases in mPFC MMP‐9 activity at 1, 3 and 24 hr after injection compared with saline controls. No changes in MMP‐9 occurred in the hippocampus or in MMP‐2 activity in either brain region. Also, no changes in mPFC MMP‐9 activity were observed 1 hr after reinstatement in animals given no extinction sessions but equivalent time off in the home cage. Finally, MMP‐3 protein levels were not different in either brain region at any of the three time points assessed. These results suggest that an elevation in MMP‐9 activity in the mPFC may contribute to synaptic remodeling important for the reactivation of a cocaine memory, or alternatively, for the modification of a competing extinction memory during reinstatement. 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Neurosci., 3:291–301, 1983; Walaas et al.: J. Neurosci., 6:954–961, 1986). PCPP‐260 has now been purified from a crude particulate fraction of bovine cerebellum, using the ionic detergent N‐lauryl sarcosine (NLS) as solubilizing agent, and monitoring the purification by silver stain and autoradiography of \u003Cjats:sup>32\u003C\u002Fjats:sup>P‐phosphorylated samples, after separation by sodium dodecyl sulfate‐polyacrylamide gel electrophoresis. Concanavalin A was found to bind to PCPP‐260, suggesting that it is a glycoprotein. PCPP‐260 was therefore extracted, retained on a column of concanavalin A‐agarose, and eluted by α‐methyl mannoside. Further chromatography on Sephacryl S‐400 yielded a preparation that was purified approximately 250‐fold relative to the initial particulate fraction and that was at least 95% pure. The protein was estimated to represent approximately 0.4% of total membrane protein in the cerebellum. Peptide mapping and phosphoamino acid analysis following phosphorylation of the protein by cAMP‐dependent protein kinase showed one major tryptic phosphopeptide containing phosphoserine. A similar, less prominent protein was also found in membranes from other brain regions but could not be detected in liver membranes. The availability of highly purified PCPP‐260 should facilitate the investigation of its possible functional roles in the nervous system.\u003C\u002Fjats:p>",{"EN":573},"Purification and characterization of PCPP‐260: A Purkinje cell‐enriched cyclic amp‐regulated membrane phosphoprotein of M\u003Csub>r\u003C\u002Fsub> 260,000",{"VOID":575},"2844000",{"VOID":577},"10.1002\u002Fsyn.890020112",[124],"https:\u002F\u002Fonlinelibrary.wiley.com\u002Fdoi\u002F10.1002\u002Fsyn.890020112",[581,603,620,635,650],{"id":582,"sortIndex":150,"researcher":23,"roles":583,"affiliations":584,"properties":596},"c64412ab-8055-4ab7-9860-3dc8aac7e628",[],[585],{"id":586,"sortIndex":24,"affiliation":587,"properties":23},"19a9b1ad-24c0-495e-9a5c-48cf16847454",{"id":588,"createTime":589,"updateTime":590,"relativeEntities":591,"slug":592,"properties":593,"entityType":43,"verifyStatus":22,"verifyTime":23,"verifyNote":23,"syncStatus":22,"languages":23,"translateLanguages":23,"viewCount":24},"484c3a66-baec-4f54-8268-6a3fade3e2bb","2024-02-08T05:17:06.609+00:00","2024-10-10T22:30:17.839+00:00",[],"Laboratory-of-Molecular-and-Cellular-Neuroscience-The-Rockefeller-University-New-York-New-York-10021",{"title":594},{"VI":595},"Laboratory of Molecular and Cellular Neuroscience, The Rockefeller University, New York, New York 10021",{"openalex":597,"orcid":599,"title":601},{"VOID":598},"A5052825834",{"VOID":600},"https:\u002F\u002Forcid.org\u002F0000-0002-4437-0893",{"EN":602},"Paul Greengard",{"id":604,"sortIndex":213,"researcher":23,"roles":605,"affiliations":606,"properties":613},"a43767eb-f9e6-475e-b618-db53a1cde5c3",[],[607],{"id":608,"sortIndex":24,"affiliation":609,"properties":23},"3a846c2e-9e4b-45c2-897f-2e40460de9ab",{"id":588,"createTime":589,"updateTime":590,"relativeEntities":610,"slug":592,"properties":611,"entityType":43,"verifyStatus":22,"verifyTime":23,"verifyNote":23,"syncStatus":22,"languages":23,"translateLanguages":23,"viewCount":24},[],{"title":612},{"VI":595},{"openalex":614,"orcid":616,"title":618},{"VOID":615},"A5032456571",{"VOID":617},"https:\u002F\u002Forcid.org\u002F0000-0002-7075-0195",{"EN":619},"Angus C. 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10.1016\u002Fj.nlm.2008.11.004",{"doi":1336},"10.1016\u002Fj.nlm.2008.11.004",{"id":23,"text":1338,"url":23,"identifiers":1339},"Zhang, 2006, Amyloid beta-protein fragment 31-35 suppresses long-term potentiation in hippocampal CA1 region of rats in vivo, Synapse, 60, 307, 10.1002\u002Fsyn.20302",{"doi":1340},"10.1002\u002Fsyn.20302",{"id":23,"text":1342,"url":23,"identifiers":1343},"Zhou, 2003, Early neuropathological Alzheimer's changes in aged individuals are accompanied by decreased cerebrospinal fluid melatonin levels, J Pineal Res, 35, 125, 10.1034\u002Fj.1600-079X.2003.00065.x",{"doi":1344},"10.1034\u002Fj.1600-079X.2003.00065.x",{"id":23,"text":1346,"url":23,"identifiers":1347},"Zucker, 2002, Short-term synaptic plasticity, Ann Rev Physiol, 64, 355, 10.1146\u002Fannurev.physiol.64.092501.114547",{"doi":1348},"10.1146\u002Fannurev.physiol.64.092501.114547",{"id":1350,"createTime":1351,"updateTime":1351,"relativeEntities":1352,"slug":1353,"properties":1354,"entityType":119,"verifyStatus":120,"verifyTime":1368,"verifyNote":122,"syncStatus":22,"languages":1369,"translateLanguages":23,"viewCount":24,"primaryUrl":1370,"fullTextUrl":23,"authors":1371,"publicationType":227,"publisherRelationship":1470,"citationCount":1502,"citationInfo":1503,"publishDate":1506,"publishYear":1507,"citationAnalyzeStatus":22,"lastCitationAnalyze":23,"indexDatabases":23,"openAccess":23,"references":1508,"isForceReanalyzing":351},"ec809b39-65c2-44a1-a293-8b2340c306cb","2024-11-29T20:57:11.275+00:00",[],"Neuroanatomic-specificity-and-time-course-of-alterations-in-rat-brain-serotonergic-pathways-induced-by-MDMA-3-4-methylenedioxymethamphetamine-Assessment-using-quantitative-autoradiography",{"mag":1355,"keywords":1357,"openalex":1358,"abstract":1360,"title":1362,"pm":1364,"doi":1366},{"VOID":1356},"2033236480",{},{"VOID":1359},"W2033236480",{"EN":1361},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\u003Cjats:p>The Widely abused “designer” durg MDMA (3,4‐methylenedioxymethamphetamine) has been shown to caused marked and long‐lasting changes in brain serotonergic systems. The present study uses quantitative in vitro autoradiography of \u003Cjats:sup>3\u003C\u002Fjats:sup>H‐paroxetine labeled 5‐HT uptake sites to assess the time‐dependent effects of MDMA on 5‐HT neurons in specific neuroanatomic loci. Following treatment with MDMA (20 mg\u002Fkg, b.i.d. for 4 days), marked decreases in 5‐HT uptake sites were observed in a number of brain regions known to receive projections of ‐5HT neurons. These regions included cerebral cortex, caudate nucleus, hippocampus, nucleus accumbens, olfactory tubercle, superior and inferior colliculi, geniculate nuclei, and most thalamic nuclei. In contrast, other areas such as the septal nuclei and some thalamic nuclei which also receive 5‐HT projections were not substantially affected by this drug. In most regions, decreases in 5‐HT uptake sites occurred within 24 hours of the last dose of MDMA and persisted at the 2 week time point. Some regions such as dorsal striatum exhibited a time‐dependent reduction with greater reductions occurring at 2 weeks rather than immediately following the MDMA treatment regimen. The density of 5‐HT uptake sites in other regions such as endopiriform nucleus and substantia nigra at the 2 week versus 18 hour time point indicated some degree of region‐specific recovery. Regions which demonstrated no significant reduction in 5‐HT uptake sites included the dorsal and median raphe nuclei, ventral tegmental area, central grey, interpeduncluar nucleus, locus coerulus, pontine reticular formation and cerebellum. Likewise, region containing 5‐HT axons of passage (e.g., indusium griseum and lateral hypothalamus) appeared to be insensitive to the neurotoxic effects of MDMA on 5‐HT neurons. Furthermore, the neurotoxic effects of MDMA showed specificity in that the catecholamine neurons labeled by \u003Cjats:sup>3\u003C\u002Fjats:sup>H‐mazindol were unaffected by the treatment regimen. These data indicate that the preferential degeneration of serotonergic neurons by MDMA is mediated primarily at 5‐HT terminal regions, whereas regions containg 5‐HT perikarya and axons of passage remain relatively unaffected. In addition, the observed time‐dependent reductions and recovery of 5‐HT uptake sites which were detected within 2 weeks of the treatment regimen in certain brain regions suggest region‐specific differences in recovery of 5‐HT systems from MDMA‐induced lesion.\u003C\u002Fjats:p>",{"EN":1363},"Neuroanatomic specificity and time course of alterations in rat brain serotonergic pathways induced by MDMA (3,4‐methylenedioxymethamphetamine): Assessment using quantitative autoradiography",{"VOID":1365},"1681594",{"VOID":1367},"10.1002\u002Fsyn.890080403","2024-11-29T20:57:11.274+00:00",[124],"https:\u002F\u002Fonlinelibrary.wiley.com\u002Fdoi\u002F10.1002\u002Fsyn.890080403",[1372,1401,1424,1445],{"id":1373,"sortIndex":213,"researcher":23,"roles":1374,"affiliations":1375,"properties":1396},"a0a3089a-6f3d-4c26-916f-7fcd2507f610",[],[1376,1386],{"id":1377,"sortIndex":24,"affiliation":1378,"properties":23},"da48505d-b018-4883-8e5a-56242722adec",{"id":1379,"createTime":1380,"updateTime":1380,"relativeEntities":1381,"slug":1382,"properties":1383,"entityType":43,"verifyStatus":22,"verifyTime":23,"verifyNote":23,"syncStatus":22,"languages":23,"translateLanguages":23,"viewCount":24},"75de8679-c598-4eb7-b376-924bf15b6394","2024-11-29T20:57:11.359+00:00",[],"Department-of-Pharmacology-Stritch-School-of-Medicine-Loyola-University-Chicago-Maywood-Illinois-60153",{"title":1384},{"EN":1385},"Department of Pharmacology, Stritch School of Medicine, Loyola University Chicago, Maywood, Illinois 60153",{"id":1387,"sortIndex":193,"affiliation":1388,"properties":23},"5b12462b-bc82-4dc2-a6be-e7d134f86e3d",{"id":1389,"createTime":1390,"updateTime":1390,"relativeEntities":1391,"slug":1392,"properties":1393,"entityType":43,"verifyStatus":22,"verifyTime":23,"verifyNote":23,"syncStatus":22,"languages":23,"translateLanguages":23,"viewCount":24},"ce692509-3885-4a01-973b-461331dd8d04","2024-11-29T20:57:11.328+00:00",[],"Neuroscience-Branch-Addiction-Research-Center-National-Institute-on-Drug-Abuse-Baltimore-Maryland-21224",{"title":1394},{"EN":1395},"Neuroscience Branch, Addiction Research Center, National Institute on Drug Abuse, Baltimore, Maryland 21224",{"openalex":1397,"title":1399},{"VOID":1398},"A5104070676",{"EN":1400},"Michael J. 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Abramson B. Katz S. andHager M.(1985)Getting high on “Ecstasy”. Newsweek April 15:96.",{},{"id":23,"text":1513,"url":23,"identifiers":1514},"Appel N. M., 1989, Fenfluramine selctively and differentially decreases the density of serotonergic nerve terminals in rat brain: Evidence from immunocytochemical studies, J. Pharmacol. Exp. Ther., 249, 928",{},{"id":23,"text":1516,"url":23,"identifiers":1517},"10.1002\u002Fsyn.890060105",{"doi":1516},{"id":23,"text":1519,"url":23,"identifiers":1520},"10.1126\u002Fscience.2893452",{"doi":1519},{"id":23,"text":1522,"url":23,"identifiers":1523},"10.1007\u002F978-94-009-1912-9_85",{"doi":1522},{"id":23,"text":1525,"url":23,"identifiers":1526},"Battaglia G., 1987, 3,4 methylenedioxymethamphetamine and 3,4 methylenedioxyamphetamine destroy serotonin terminals in rat brain: Quantification of neurodegeneration by measurement of 3H‐paroxetine labeled serotonin uptake sites, J. Pharmacol. Exp., Ther., 242, 911",{},{"id":23,"text":1528,"url":23,"identifiers":1529},"10.1016\u002F0091-3057(88)90155-4",{"doi":1528},{"id":23,"text":1531,"url":23,"identifiers":1532},"Commins D. L., 1987, Biochemical and histological evidence that methylenedioxymethamphetamine (MDMA) is toxic to neurons in rat brain, J. Pharmacol. Exp. Ther., 241, 338",{},{"id":23,"text":1534,"url":23,"identifiers":1535},"D'Amato R. J., 1987, Selective labelling of serotonin uptake sites in rat brain by 3H‐citalopram constrasted to labelling of multiple sites by 3H‐imipramine, J. Pharmacol. Exp. Ther., 242, 364",{},{"id":23,"text":1537,"url":23,"identifiers":1538},"10.1002\u002Fsyn.890010513",{"doi":1537},{"id":23,"text":1540,"url":23,"identifiers":1541},"10.1016\u002F0006-8993(89)90562-3",{"doi":1540},{"id":23,"text":1543,"url":23,"identifiers":1544},"10.1111\u002Fj.1749-6632.1978.tb31521.x",{"doi":1543},{"id":23,"text":1546,"url":23,"identifiers":1547},"Gertz K. R.(1986)The agony of ecstasy. Science Digest February:27.",{},{"id":23,"text":1549,"url":23,"identifiers":1550},"Insel T. R., 1989, 3,4 Methylenedioxymethamphetamine (“Ecstasy”) selectively destroys brain serotonin terminals in Rhesus monkeys, J. Pharmacol. Exp. Ther., 249, 713",{},{"id":23,"text":1552,"url":23,"identifiers":1553},"Javitch J. A., 1985, Differential visualization of dopamine and norepinephrine uptake sites in rat brain using 3H‐mazindol autoradiography, J. Neurosci., 5, 1513, 10.1523\u002FJNEUROSCI.05-06-01513.1985",{"doi":1554},"10.1523\u002FJNEUROSCI.05-06-01513.1985",{"id":23,"text":1556,"url":23,"identifiers":1557},"10.1002\u002Fsyn.890010204",{"doi":1556},{"id":23,"text":1559,"url":23,"identifiers":1560},"10.1016\u002F0006-8993(89)90122-4",{"doi":1559},{"id":23,"text":1562,"url":23,"identifiers":1563},"Kovachich G. B., 1990, Effects of repeated administration of antidepressants on serotonin (5‐HT) uptake sites measured using 3H‐cyanoimipramine autoradiography, Soc. Neurosci. Abstr., 16, 1040",{},{"id":23,"text":1565,"url":23,"identifiers":1566},"10.1016\u002F0014-4886(88)90075-1",{"doi":1565},{"id":23,"text":1568,"url":23,"identifiers":1569},"10.1097\u002F00004714-198712001-00002",{"doi":1568},{"id":23,"text":1571,"url":23,"identifiers":1572},"10.1111\u002Fj.1749-6632.1978.tb31531.x",{"doi":1571},{"id":23,"text":1574,"url":23,"identifiers":1575},"O'Hearn E., 1988, Methylenedioxyamphetamine (MDA) and methylenedioxymethamphetamine (MDMA) cause ablation of serotonergic axons terminals in forebrain: Immunocytochemical evidence for neurotoxicity, J. Neurosci., 8, 2788, 10.1523\u002FJNEUROSCI.08-08-02788.1988",{"doi":1576},"10.1523\u002FJNEUROSCI.08-08-02788.1988",{"id":23,"text":1578,"url":23,"identifiers":1579},"Paxinos G., 1982, The Rat in Stereotaxic Coordinates",{},{"id":23,"text":1581,"url":23,"identifiers":1582},"10.1126\u002Fscience.4023719",{"doi":1581},{"id":23,"text":1584,"url":23,"identifiers":1585},"Ricaurte G. A., 1988, (±) 3,4‐methylenedioxymethamphetamine selectively damages central serotonergic neurons in nonhuman primates, JAMA, 260, 51, 10.1001\u002Fjama.1988.03410010059035",{"doi":1586},"10.1001\u002Fjama.1988.03410010059035",{"id":23,"text":1588,"url":23,"identifiers":1589},"10.1111\u002Fj.1749-6632.1978.tb31525.x",{"doi":1588},{"id":23,"text":1591,"url":23,"identifiers":1592},"10.1016\u002F0006-2952(87)90566-1",{"doi":1591},{"id":23,"text":1594,"url":23,"identifiers":1595},"10.1016\u002F0306-4522(81)90146-9",{"doi":1594},{"id":23,"text":1597,"url":23,"identifiers":1598},"10.1016\u002F0028-3908(87)90117-1",{"doi":1597},{"id":23,"text":1600,"url":23,"identifiers":1601},"10.1002\u002Fcne.901860408",{"doi":1600},{"id":23,"text":1603,"url":23,"identifiers":1604},"10.1111\u002Fj.1749-6632.1978.tb31534.x",{"doi":1603},{"id":23,"text":1606,"url":23,"identifiers":1607},"Zaczek R., 1989, Effects of repeated fenfluramine administration on indices of monoamine function in rat brain: Pharmacokinetic, dose response, regional specificity and time course data, J. Pharmacol. Exp. Ther., 253, 104",{},{"id":1609,"createTime":1610,"updateTime":1610,"relativeEntities":1611,"slug":1612,"properties":1613,"entityType":119,"verifyStatus":120,"verifyTime":1627,"verifyNote":122,"syncStatus":22,"languages":1628,"translateLanguages":23,"viewCount":24,"primaryUrl":1629,"fullTextUrl":23,"authors":1630,"publicationType":227,"publisherRelationship":1703,"citationCount":1735,"citationInfo":1736,"publishDate":1738,"publishYear":1739,"citationAnalyzeStatus":22,"lastCitationAnalyze":23,"indexDatabases":23,"openAccess":23,"references":1740,"isForceReanalyzing":351},"f33b09ca-8d7f-4966-88f9-8f7cf1dc4d2b","2024-11-29T20:57:09.159+00:00",[],"Effect-of-destruction-of-serotonin-neurons-on-basal-and-fenfluramine-induced-serotonin-release-in-striatum",{"mag":1614,"keywords":1616,"openalex":1617,"abstract":1619,"title":1621,"pm":1623,"doi":1625},{"VOID":1615},"2000712316",{},{"VOID":1618},"W2000712316",{"EN":1620},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\u003Cjats:p>This study examined the relationship between the magnitude of tissue serotonin (5‐HT)depletion produced by treatment with the neurotoxin 5,7‐dihydroxytryptamine (5,7) and basal and fenfluramine‐induced 5‐HT release in the striatum. Separate groups of rats were treated with either vehicle or 5,7‐DHT (100μ 76% striatal 5‐HT depletion; or 200μ 93% styriatal 5‐HT depletion). four weeks after treatment 5‐HT release was measured in the ventral striatum using in vivo microdialysis in animals anesthetized with chloral hydrate. Basal 5‐HT levels were not significantly altered in any lesion group, whereas basal 5‐hydroxyindoleacetic acid levels were dosedependently reduced by 5,7‐DHT. In contrast, the increase of 5‐HT release produced by fenfluramine treatement (10 mg\u002Fkg) wa diminished significantly after 5‐HT neuronal destruction in correlation with the reduction of striatal tissue 5‐HT content. Fractional 5‐HT efflux, a measure of the 5‐HT release from surviving striatal nerve terminals, was also significantly elevated when tissue depletion of 5‐HT exceeded 95%. This study suggests that compensatory mechanisms may enable surviving 5‐HT terminals to maintain basal 5‐HT levels in th striatum with as little as 5% of the terminals remaining, but those mechanisms are not sufficient to allow the damaged system to respond to a pharmacological challenge. © 1995 Wiley‐Liss, Inc.\u003C\u002Fjats:p>",{"EN":1622},"Effect of destruction of serotonin neurons on basal and fenfluramine‐induced serotonin release in striatum",{"VOID":1624},"7570349",{"VOID":1626},"10.1002\u002Fsyn.890200202","2024-11-29T20:57:09.155+00:00",[124],"https:\u002F\u002Fonlinelibrary.wiley.com\u002Fdoi\u002F10.1002\u002Fsyn.890200202",[1631,1652,1669,1686],{"id":1632,"sortIndex":24,"researcher":23,"roles":1633,"affiliations":1634,"properties":1645},"0d727549-0c64-43b1-b187-69642352eb45",[],[1635],{"id":1636,"sortIndex":24,"affiliation":1637,"properties":23},"430130ad-ce0b-4e8c-b73f-f8b017f36da4",{"id":1638,"createTime":1639,"updateTime":1639,"relativeEntities":1640,"slug":1641,"properties":1642,"entityType":43,"verifyStatus":22,"verifyTime":23,"verifyNote":23,"syncStatus":22,"languages":23,"translateLanguages":23,"viewCount":24},"a9a4aeaa-332a-4f2c-8e48-0f28142d1717","2024-11-29T20:57:09.223+00:00",[],"Departments-of-Psychiatry-and-Pharmacology-Institure-of-Neurological-Sciences-University-of-Pennsylvania-Philadelphia-Pennsylvania-19194-2649",{"title":1643},{"EN":1644},"Departments of Psychiatry and Pharmacology, Institure of Neurological Sciences, University of Pennsylvania, Philadelphia, Pennsylvania 19194-2649",{"openalex":1646,"orcid":1648,"title":1650},{"VOID":1647},"A5013964605",{"VOID":1649},"https:\u002F\u002Forcid.org\u002F0000-0001-5684-6716",{"EN":1651},"Lynn G. 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M., 1986, Handbook of Physiology, Vol. 4, Intrinsic Regulatory Systems of the Brain, 677",{},{"id":23,"text":1799,"url":23,"identifiers":1800},"10.1016\u002F0165-0270(89)90062-9",{"doi":1799},{"id":23,"text":1802,"url":23,"identifiers":1803},"10.1016\u002F0166-2236(90)90112-N",{"doi":1802},{"id":23,"text":1805,"url":23,"identifiers":1806},"10.1111\u002Fj.1749-6632.1992.tb24525.x",{"doi":1805},{"id":1808,"createTime":1809,"updateTime":1809,"relativeEntities":1810,"slug":1811,"properties":1812,"entityType":119,"verifyStatus":120,"verifyTime":1809,"verifyNote":122,"syncStatus":22,"languages":1825,"translateLanguages":23,"viewCount":24,"primaryUrl":1826,"fullTextUrl":23,"authors":1827,"publicationType":227,"publisherRelationship":1860,"citationCount":1892,"citationInfo":1893,"publishDate":1895,"publishYear":1896,"citationAnalyzeStatus":22,"lastCitationAnalyze":23,"indexDatabases":23,"openAccess":23,"references":1897,"isForceReanalyzing":351},"d6680afe-d326-49a6-a9da-9a92e7b65e60","2024-11-29T20:57:09.856+00:00",[],"Autoradiographic-localization-of-sup-3-sup-H-paroxetine-labeled-serotonin-uptake-sites-in-rat-brain",{"mag":1813,"keywords":1815,"openalex":1816,"abstract":1818,"title":1820,"pm":1822,"doi":1824},{"VOID":1814},"1999320578",{},{"VOID":1817},"W1999320578",{"EN":1819},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\u003Cjats:p>Paroxetine is a potent and selective inhibitor of serotonin uptake into neurons. Serotonin uptake sites have been identified, localized, and quantified in rat brain by autoradiography with \u003Cjats:sup>3\u003C\u002Fjats:sup>H‐paroxetine; \u003Cjats:sup>3\u003C\u002Fjats:sup>H‐paroxetine binding in slide‐mounted sections of rat forebrain was of high affinity (K\u003Cjats:sub>D\u003C\u002Fjats:sub> = 10 pM) and the inhibition affinity constant (K\u003Cjats:sub>i\u003C\u002Fjats:sub>) values of various drugs in competing \u003Cjats:sup>3\u003C\u002Fjats:sup>H‐paroxetine binding significantly correlated with their reported potencies in inhibiting synaptosomal serotonin uptake. Serotonin uptake sites labeled by \u003Cjats:sup>3\u003C\u002Fjats:sup>H‐paroxetine were highly concentrated in the dorsal and median raphe nuclei, central gray, superficial layer of the superior colliculus, lateral septal nucleus, paraventricular nucleus of the thalamus, and the islands of Calleja. High concentrations of \u003Cjats:sup>3\u003C\u002Fjats:sup>H‐paroxetine binding sites were found in brainstem areas containing dopamine (substantia nigra and ventral tegmental area) and norepinephrine (locus coeruleus) cell bodies. Moderate concentrations of \u003Cjats:sup>3\u003C\u002Fjats:sup>H‐paroxetine binding sites were present in laminae I and IV of the frontal parietal cortex, primary olfactory cortex, olfactory tubercle, regions of the basal ganglia, septum, amygdala, thalamus, hypothalamus, hippocampus, and some brainstem areas including the interpeduncular, trigeminal, and parabrachial nuclei. Lower densities of \u003Cjats:sup>3\u003C\u002Fjats:sup>H‐paroxetine binding sites were found in other regions of the neocortex and very low to nonsignificant levels of binding were present in white matter tracts and in the cerebellum. Lesioning of serotonin neurons with 3,4‐methylenedioxyamphetamine caused large decreases in \u003Cjats:sup>3\u003C\u002Fjats:sup>H‐paroxetine binding. The autoradiographic distribution of \u003Cjats:sup>3\u003C\u002Fjats:sup>H‐paroxetine binding sites in rat brain corresponds extremely well to the distribution of serotonin terminals and cell bodies as well as with the pharmacological sites of action of serotonin.\u003C\u002Fjats:p>",{"EN":1821},"Autoradiographic localization of \u003Csup>3\u003C\u002Fsup>H‐paroxetine‐labeled serotonin uptake sites in rat brain",{"VOID":1823},"2975068",{"VOID":1537},[124],"https:\u002F\u002Fonlinelibrary.wiley.com\u002Fdoi\u002F10.1002\u002Fsyn.890010513",[1828,1845],{"id":1829,"sortIndex":24,"researcher":23,"roles":1830,"affiliations":1831,"properties":1842},"be9e4161-9d71-44c8-ac0c-970810498797",[],[1832],{"id":1833,"sortIndex":24,"affiliation":1834,"properties":23},"a7c2fc98-77cc-46d5-a7af-6113347dba5d",{"id":1835,"createTime":1836,"updateTime":1836,"relativeEntities":1837,"slug":1838,"properties":1839,"entityType":43,"verifyStatus":22,"verifyTime":23,"verifyNote":23,"syncStatus":22,"languages":23,"translateLanguages":23,"viewCount":24},"dd1f1b18-c428-4e78-8f1a-de08b54095ee","2024-11-29T20:57:09.874+00:00",[],"Neuroscience-Branch-Addiction-Research-Center-National-Institute-on-Drug-Abuse-Alcohol-Drug-Abuse-and-Mental-Health-Administration-Baltimore-Maryland-21224",{"title":1840},{"EN":1841},"Neuroscience Branch, Addiction Research Center, National Institute on Drug Abuse, Alcohol, Drug Abuse, and Mental Health Administration, Baltimore, Maryland 21224",{"openalex":1843,"title":1844},{"VOID":1442},{"EN":1444},{"id":1846,"sortIndex":193,"researcher":23,"roles":1847,"affiliations":1848,"properties":1855},"c0ec25b0-308b-4a1a-b1ef-d5cbfa85a73b",[],[1849],{"id":1850,"sortIndex":24,"affiliation":1851,"properties":23},"9dce49b2-b66f-49b6-b75f-31bf227059d4",{"id":1835,"createTime":1836,"updateTime":1836,"relativeEntities":1852,"slug":1838,"properties":1853,"entityType":43,"verifyStatus":22,"verifyTime":23,"verifyNote":23,"syncStatus":22,"languages":23,"translateLanguages":23,"viewCount":24},[],{"title":1854},{"EN":1841},{"openalex":1856,"title":1858},{"VOID":1857},"A5020008994",{"EN":1859},"Brian L. Kuyatt",{"url":23,"publisher":1861,"properties":1886},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":1862,"slug":10,"properties":1863,"entityType":21,"verifyStatus":22,"verifyTime":23,"verifyNote":23,"syncStatus":22,"languages":23,"translateLanguages":23,"viewCount":24,"subjectFields":1869,"manageAffiliations":1870,"indexDatabases":1871,"url":95,"thumbnailPath":23,"statistic":23,"gsStatistic":23,"type":23,"analyzePriority":23},[],{"country":1864,"issn":1865,"introduce":1866,"eissn":1867,"title":1868},{"VOID":13},{"VOID":15},{"EN":17},{"VOID":19},{"EN":10},[],[],[1872,1879],{"id":58,"indexDatabase":1873,"url":73,"indexYears":23,"academicFieldIds":1878,"indexDatabaseRanking":23},{"id":60,"createTime":61,"updateTime":62,"relativeEntities":1874,"label":1875,"description":1876,"key":69,"publicationTags":1877,"standard":23},[],{"EN":65,"VI":65},{"VI":67,"EN":68},[71,72],[75],{"id":77,"indexDatabase":1880,"url":90,"indexYears":91,"academicFieldIds":1885,"indexDatabaseRanking":94},{"id":79,"createTime":80,"updateTime":81,"relativeEntities":1881,"label":1882,"description":1883,"key":87,"publicationTags":1884,"standard":23},[],{"EN":84,"VI":84},{"EN":84,"VI":86},[89],[93],{"volume":1887,"pages":1888,"issue":1890},{"VOID":699},{"VOID":1889},"488-496",{"VOID":1891},"5",129,{"total":1892,"publishYear":23,"statisticByYear":1894},{"2013":213,"2014":193,"2016":193,"2018":193},"1987-01-01",1987,[1898,1901,1904,1907,1910,1913,1916,1919,1922,1925,1928,1931,1934,1937,1940,1943,1946,1949,1952,1955,1958,1961,1964,1967,1970,1973,1976,1979,1982,1985,1988,1991,1994,1997,2000,2003,2006,2009,2012,2015,2018,2021,2023,2026,2029,2032,2035,2037,2040,2043,2046,2049,2052],{"id":23,"text":1899,"url":23,"identifiers":1900},"Antonaccio M. J., 1977, Cardiovascular Pharmacology, 131",{},{"id":23,"text":1902,"url":23,"identifiers":1903},"Aprison M. H., 1975, Serotonergic and cholinergic mechanisms during disruption of approach and avoidance behavior, Fed. Proc., 34, 1813",{},{"id":23,"text":1905,"url":23,"identifiers":1906},"10.1007\u002FBF00426037",{"doi":1905},{"id":23,"text":1908,"url":23,"identifiers":1909},"Battaglia G. Yeh S. Y. O'Hearn E. Molliver M. E. Kuhar M. J.andDe Souza E. B.3 4‐Methylenedioxymethamphetamine (MDMA) and 3 4‐Methylenedioxyamphetamine (MDA) preferentially destroy serotonin terminals in rat brain: quantification of neurodegeneration by measurement of3H‐paroxetine‐labeled serotonin uptake sites.J. Pharmacol. Exp. Ther. in press.",{},{"id":23,"text":1911,"url":23,"identifiers":1912},"Blundell J. E., 1977, Is there a role for serotonin (5‐hydroxytryptamine) in feeding?, Int. J. 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H.Selective labeling of serotonin uptake sites in rat brain by3H‐citalopram contrasted to labeling of multiple sites by3H‐imipramine.J. Pharmacol. Exp. Ther. in press.",{},{"id":23,"text":1935,"url":23,"identifiers":1936},"10.1016\u002F0361-9230(83)90169-7",{"doi":1935},{"id":23,"text":1938,"url":23,"identifiers":1939},"10.1111\u002Fj.1476-5381.1978.tb07785.x",{"doi":1938},{"id":23,"text":1941,"url":23,"identifiers":1942},"10.1073\u002Fpnas.80.12.3836",{"doi":1941},{"id":23,"text":1944,"url":23,"identifiers":1945},"Galzin A. M., 1985, Interaction between tricyclic and nontricyclic 5‐hydroxytryptamine uptake inhibitors and the presynaptic 5‐hydroxytryptamine inhibitory autoreceptor in the rat hypothalamus, J. Pharmacol. Exp. Ther., 235, 200",{},{"id":23,"text":1947,"url":23,"identifiers":1948},"Geller I., 1974, Attenuation of conflict behavior with cinanserin, a serotonin antagonist: Reversal of the effect with 5‐hydroxytryptophan and alpha‐methyltryptamine, Res. Commun. Chem. Pathol. Pharmacol., 7, 165",{},{"id":23,"text":1950,"url":23,"identifiers":1951},"10.1016\u002F0024-3205(80)90368-9",{"doi":1950},{"id":23,"text":1953,"url":23,"identifiers":1954},"Gibbons J. L., 1979, Effects of quipazine, fluoxetine, and fenfluramine on muricide in rats, Fed. Proc., 38, 257",{},{"id":23,"text":1956,"url":23,"identifiers":1957},"10.1016\u002F0014-2999(85)90668-5",{"doi":1956},{"id":23,"text":1959,"url":23,"identifiers":1960},"10.1016\u002FS0278-5846(82)80178-4",{"doi":1959},{"id":23,"text":1962,"url":23,"identifiers":1963},"10.1016\u002F0014-2999(85)90135-9",{"doi":1962},{"id":23,"text":1965,"url":23,"identifiers":1966},"10.1111\u002Fj.1749-6632.1977.tb41880.x",{"doi":1965},{"id":23,"text":1968,"url":23,"identifiers":1969},"10.1016\u002F0006-8993(72)90372-1",{"doi":1968},{"id":23,"text":1971,"url":23,"identifiers":1972},"Kuhar M. J., 1973, Selective accumulation of 3H‐serotonin by nerve terminals of raphe neurons: An autoradiography study, Nature, 241, 187",{},{"id":23,"text":1974,"url":23,"identifiers":1975},"10.1111\u002Fj.1600-0404.1978.tb04502.x",{"doi":1974},{"id":23,"text":1977,"url":23,"identifiers":1978},"10.1016\u002F0006-8993(78)90610-8",{"doi":1977},{"id":23,"text":1980,"url":23,"identifiers":1981},"10.1016\u002F0014-2999(83)90321-7",{"doi":1980},{"id":23,"text":1983,"url":23,"identifiers":1984},"10.1007\u002FBF02412117",{"doi":1983},{"id":23,"text":1986,"url":23,"identifiers":1987},"10.1016\u002F0304-3959(77)90083-5",{"doi":1986},{"id":23,"text":1989,"url":23,"identifiers":1990},"Meyerson B. J., 1978, Biological Determinants of Sexual Behavior, 521",{},{"id":23,"text":1992,"url":23,"identifiers":1993},"Myers R. D., 1978, Serotonin in Health and Disease, Vol. II. Psychological Regulation and Pharmacological Action, 1",{},{"id":23,"text":1995,"url":23,"identifiers":1996},"10.1007\u002FBF00498988",{"doi":1995},{"id":23,"text":1998,"url":23,"identifiers":1999},"O'Hearn E., 1986, Systemic MDA and MDMA, psychotropic substituted amphetamines produce serotonin neurotoxicity, Soc. Neurosci. Abstr., 12, 1233",{},{"id":23,"text":2001,"url":23,"identifiers":2002},"10.1016\u002F0304-3940(81)90315-3",{"doi":2001},{"id":23,"text":2004,"url":23,"identifiers":2005},"10.1016\u002F0006-8993(77)90847-2",{"doi":2004},{"id":23,"text":2007,"url":23,"identifiers":2008},"10.1016\u002F0306-4522(81)90050-6",{"doi":2007},{"id":23,"text":2010,"url":23,"identifiers":2011},"10.1016\u002FB978-0-12-547620-1.50007-2",{"doi":2010},{"id":23,"text":2013,"url":23,"identifiers":2014},"10.1016\u002F0014-2999(82)90146-7",{"doi":2013},{"id":23,"text":2016,"url":23,"identifiers":2017},"10.1016\u002F0006-8993(83)91026-0",{"doi":2016},{"id":23,"text":2019,"url":23,"identifiers":2020},"10.1212\u002FWNL.36.4.556",{"doi":2019},{"id":23,"text":1581,"url":23,"identifiers":2022},{"doi":1581},{"id":23,"text":2024,"url":23,"identifiers":2025},"Saavedra J. M., 1977, Distribution of serotonin and synthesizing enzymes in discrete areas of the brain, Fed. Proc., 36, 2134",{},{"id":23,"text":2027,"url":23,"identifiers":2028},"10.1016\u002F0024-3205(75)90128-9",{"doi":2027},{"id":23,"text":2030,"url":23,"identifiers":2031},"10.1111\u002Fj.1471-4159.1985.tb04019.x",{"doi":2030},{"id":23,"text":2033,"url":23,"identifiers":2034},"10.1126\u002Fscience.7079769",{"doi":2033},{"id":23,"text":1594,"url":23,"identifiers":2036},{"doi":1594},{"id":23,"text":2038,"url":23,"identifiers":2039},"10.1056\u002FNEJM197701132960203",{"doi":2038},{"id":23,"text":2041,"url":23,"identifiers":2042},"10.1016\u002F0014-2999(79)90110-9",{"doi":2041},{"id":23,"text":2044,"url":23,"identifiers":2045},"10.1152\u002Fphysrev.1978.58.4.905",{"doi":2044},{"id":23,"text":2047,"url":23,"identifiers":2048},"10.1111\u002Fj.1600-0773.1975.tb00781.x",{"doi":2047},{"id":23,"text":2050,"url":23,"identifiers":2051},"10.1016\u002F0091-3057(78)90362-3",{"doi":2050},{"id":23,"text":2053,"url":23,"identifiers":2054},"Yeh S. Y., 1986, Effects of MDA and MDMA (ecstasy) on brain monoaminergic systems: In vivo studies, Soc. Neurosci. Abstr., 12, 1233",{},{"id":2056,"createTime":2057,"updateTime":2057,"relativeEntities":2058,"slug":2059,"properties":2060,"entityType":119,"verifyStatus":120,"verifyTime":2074,"verifyNote":122,"syncStatus":22,"languages":2075,"translateLanguages":23,"viewCount":24,"primaryUrl":2076,"fullTextUrl":23,"authors":2077,"publicationType":227,"publisherRelationship":2134,"citationCount":2166,"citationInfo":2167,"publishDate":2170,"publishYear":2171,"citationAnalyzeStatus":22,"lastCitationAnalyze":23,"indexDatabases":23,"openAccess":23,"references":2172,"isForceReanalyzing":351},"879e2459-c0c0-4334-abc5-dc66cbad06cf","2024-09-11T20:48:48.330+00:00",[],"Functional-analysis-of-MOR-1-splice-variants-of-the-mouse-mu-opioid-receptor-gene-i-Oprm-i-",{"mag":2061,"keywords":2063,"openalex":2064,"abstract":2066,"title":2068,"pm":2070,"doi":2072},{"VOID":2062},"2111914919",{},{"VOID":2065},"W2111914919",{"EN":2067},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\u003Cjats:p>A series of mu opioid receptor gene \u003Cjats:italic>Oprm\u003C\u002Fjats:italic> splice variants have been reported that differ only at their C‐terminus. These variants all contain exons 1, 2, and 3 of the gene, the exons responsible for coding all seven transmembrane domains. Whereas MOR‐1 also has exon 4 that encodes for an additional 12 amino acids at the tip of the C‐terminus, the other MOR‐1 variants have unique amino acid sequences distinct from those in MOR‐1 due to alternative splicing. All these variants are mu‐selective in binding assays. The current study explored the ability of these variants to stimulate [\u003Cjats:sup>35\u003C\u002Fjats:sup>S]GTPγS binding to assess them functionally. Only mu opioids stimulated [\u003Cjats:sup>35\u003C\u002Fjats:sup>S]GTPγS binding. Among the mu opioids we noted marked differences in their maximal stimulation among the clones. This was most prominent with β‐endorphin, which stimulated [\u003Cjats:sup>35\u003C\u002Fjats:sup>S]GTPγS binding in the MOR‐1E expressing cells to a greater degree than [D‐Ala\u003Cjats:sup>2\u003C\u002Fjats:sup>,MePhe\u003Cjats:sup>4\u003C\u002Fjats:sup>,Gly(ol)\u003Cjats:sup>5\u003C\u002Fjats:sup>]enkephalin (DAMGO; 130%) and was far less effective than DAMGO in MOR‐1C cells (44%). The rank order of maximal stimulation of the drugs varied among the clones as well. Dynorphin A, β‐endorphin and morphine were most effective in stimulating [\u003Cjats:sup>35\u003C\u002Fjats:sup>S]GTPγS binding in MOR‐1E, while M6G and fentanyl were most effective in MOR‐1 expressing cells. The potency (EC\u003Cjats:sub>50\u003C\u002Fjats:sub>) of some of the drugs also varied extensively among the clones, with a poor correlation between the potency of the drugs to stimulate [\u003Cjats:sup>35\u003C\u002Fjats:sup>S]GTPγS binding and their binding affinity. Together, these findings reveal marked functional differences among the variants that only can be explained by their structural differences at the tip of their C‐terminus. Synapse 51:11–18, 2004. © 2003 Wiley‐Liss, Inc.\u003C\u002Fjats:p>",{"EN":2069},"Functional analysis of MOR‐1 splice variants of the mouse mu opioid receptor gene \u003Ci>Oprm\u003C\u002Fi>",{"VOID":2071},"14579421",{"VOID":2073},"10.1002\u002Fsyn.10277","2024-09-11T20:48:48.329+00:00",[124],"https:\u002F\u002Fonlinelibrary.wiley.com\u002Fdoi\u002F10.1002\u002Fsyn.10277",[2078,2099,2117],{"id":2079,"sortIndex":213,"researcher":23,"roles":2080,"affiliations":2081,"properties":2092},"975ac327-03ca-4d60-a674-45e44b6c870e",[],[2082],{"id":2083,"sortIndex":24,"affiliation":2084,"properties":23},"0ad9d8f6-3ca1-4094-b858-b49028757cd5",{"id":2085,"createTime":2086,"updateTime":2086,"relativeEntities":2087,"slug":2088,"properties":2089,"entityType":43,"verifyStatus":22,"verifyTime":23,"verifyNote":23,"syncStatus":22,"languages":23,"translateLanguages":23,"viewCount":24},"427d1a9c-1a48-457e-b05c-10d0882f8a56","2024-09-11T20:48:48.380+00:00",[],"Laboratory-of-Molecular-Neuropharmacology-Memorial-Sloan-Kettering-Cancer-Center-and-Program-in-Neuroscience-The-Weill-Graduate-School-of-Medical-Sciences-of-Cornell-University-New-York-New-York-10021",{"title":2090},{"EN":2091},"Laboratory of Molecular Neuropharmacology, Memorial Sloan‐Kettering Cancer Center, and Program in Neuroscience, The Weill Graduate School of Medical Sciences of Cornell University, New York, New York 10021",{"openalex":2093,"orcid":2095,"title":2097},{"VOID":2094},"A5081392679",{"VOID":2096},"https:\u002F\u002Forcid.org\u002F0000-0003-0060-6996",{"EN":2098},"Gavril W. 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Because previous research has demonstrated that physical activity can ameliorate nigrostriatal injury, this study investigated whether voluntary exercise in rats can alter the monoaminergic damage resulting from a neurotoxic mAMPH binge. Adult male rats were allowed constant access to running wheels or kept in nonwheel cages for three weeks, then given a binge dosing regimen of mAMPH or saline. The rats were returned to their original environments for three additional weeks post‐mAMPH. [\u003Cjats:sup>125\u003C\u002Fjats:sup>I]RTI‐55 binding and autoradiography was used to quantify dopamine transporters (DAT), and radioimmunocytochemistry was used to quantify striatal tyrosine hydroxylase (TH). Binge mAMPH treatment significantly reduced striatal DAT and TH in a regionally specific pattern; with greatest effects in ventral caudate‐putamen (CP) and relative sparing of the nucleus accumbens septi (NAc). The effects of mAMPH on striatal DAT and TH were ameliorated in the running, compared to the sedentary, animals. Also, mAMPH was found to reduce [\u003Cjats:sup>125\u003C\u002Fjats:sup>I]RTI‐55 binding to serotonin transporters (SERT) in frontoparietal cortex, and this too was significantly attenuated by exercise. Additional correlational analyses showed that the post‐mAMPH running of individual animals predicted the amelioration of striatal DAT and TH as well as frontoparietal SERT. Overall, voluntary exercise significantly diminished mAMPH‐induced forebrain monoaminergic damage. The significant correlations between post‐mAMPH exercise and markers of monoaminergic terminal integrity provide novel evidence that voluntary exercise may exert beneficial effects on behavior in recovering mAMPH addicts. 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