Methamphetamine treatment during development attenuates the dopaminergic deficits caused by subsequent high-dose methamphetamine administration
Administration of high doses of methamphetamine (METH) causes persistent dopaminergic deficits in both nonhuman preclinical models and METH‐dependent persons. Noteworthy, adolescent [i.e., postnatal day (PND) 40] rats are less susceptible to this damage than young adult (PND90) rats. In addition, bi...
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| Veröffentlicht in: | Synapse (New York, N.Y.) N.Y.), 2011-08, Vol.65 (8), p.771-777 |
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| creator | Mcfadden, Lisa M. Hoonakker, Amanda J. Vieira-Brock, Paula L. Stout, Kristen A. Sawada, Nicole M. Ellis, Jonathan D. Allen, Scott C. Walters, Elliot T. Nielsen, Shannon M. Gibb, James W. Alburges, Mario E. Wilkins, Diana G. Hanson, Glen R. Fleckenstein, Annette E. |
| description | Administration of high doses of methamphetamine (METH) causes persistent dopaminergic deficits in both nonhuman preclinical models and METH‐dependent persons. Noteworthy, adolescent [i.e., postnatal day (PND) 40] rats are less susceptible to this damage than young adult (PND90) rats. In addition, biweekly treatment with METH, beginning at PND40 and continuing throughout development, prevents the persistent dopaminergic deficits caused by a “challenge” high‐dose METH regimen when administered at PND90. Mechanisms underlying this “resistance” were thus investigated. Results revealed that biweekly METH treatment throughout development attenuated both the acute and persistent deficits in VMAT2 function, as well as the acute hyperthermia, caused by a challenge METH treatment. Pharmacokinetic alterations did not appear to contribute to the protection afforded by the biweekly treatment. Maintenance of METH‐induced hyperthermia abolished the protection against both the acute and persistent VMAT2‐associated deficits suggesting that alterations in thermoregulation were caused by exposure of rats to METH duringdevelopment. These findings suggest METH during development prevents METH‐induced hyperthermia and the consequent METH‐related neurotoxicity. Synapse 2011. © 2011 Wiley‐Liss, Inc. |
| doi_str_mv | 10.1002/syn.20902 |
| format | Article |
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Noteworthy, adolescent [i.e., postnatal day (PND) 40] rats are less susceptible to this damage than young adult (PND90) rats. In addition, biweekly treatment with METH, beginning at PND40 and continuing throughout development, prevents the persistent dopaminergic deficits caused by a “challenge” high‐dose METH regimen when administered at PND90. Mechanisms underlying this “resistance” were thus investigated. Results revealed that biweekly METH treatment throughout development attenuated both the acute and persistent deficits in VMAT2 function, as well as the acute hyperthermia, caused by a challenge METH treatment. Pharmacokinetic alterations did not appear to contribute to the protection afforded by the biweekly treatment. Maintenance of METH‐induced hyperthermia abolished the protection against both the acute and persistent VMAT2‐associated deficits suggesting that alterations in thermoregulation were caused by exposure of rats to METH duringdevelopment. These findings suggest METH during development prevents METH‐induced hyperthermia and the consequent METH‐related neurotoxicity. Synapse 2011. © 2011 Wiley‐Liss, Inc.</description><identifier>ISSN: 0887-4476</identifier><identifier>ISSN: 1098-2396</identifier><identifier>EISSN: 1098-2396</identifier><identifier>DOI: 10.1002/syn.20902</identifier><identifier>PMID: 21190217</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Adolescence ; Animals ; Body Temperature Regulation - drug effects ; Brain - drug effects ; Brain - metabolism ; Central Nervous System Stimulants - administration & dosage ; Central Nervous System Stimulants - adverse effects ; Chromatography, Gas ; Development ; Dopamine ; Dopamine - metabolism ; Fever - chemically induced ; Growth and Development - drug effects ; Hyperthermia ; Male ; Mass Spectrometry ; Methamphetamine ; Methamphetamine - administration & dosage ; Methamphetamine - adverse effects ; Neurotoxicity ; Pharmacokinetics ; Rats ; Rats, Sprague-Dawley ; Synapses ; Thermoregulation ; Vesicular amine transporter ; Vesicular Monoamine Transport Proteins - biosynthesis ; vesicular monoamine transporter-2</subject><ispartof>Synapse (New York, N.Y.), 2011-08, Vol.65 (8), p.771-777</ispartof><rights>Copyright © 2011 Wiley‐Liss, Inc.</rights><rights>Copyright © 2011 Wiley-Liss, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4852-526926f043c661c9d387990c620af4de843f4da734184e4bf5de8507659371ce3</citedby><cites>FETCH-LOGICAL-c4852-526926f043c661c9d387990c620af4de843f4da734184e4bf5de8507659371ce3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fsyn.20902$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fsyn.20902$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>230,314,776,780,881,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21190217$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mcfadden, Lisa M.</creatorcontrib><creatorcontrib>Hoonakker, Amanda J.</creatorcontrib><creatorcontrib>Vieira-Brock, Paula L.</creatorcontrib><creatorcontrib>Stout, Kristen A.</creatorcontrib><creatorcontrib>Sawada, Nicole M.</creatorcontrib><creatorcontrib>Ellis, Jonathan D.</creatorcontrib><creatorcontrib>Allen, Scott C.</creatorcontrib><creatorcontrib>Walters, Elliot T.</creatorcontrib><creatorcontrib>Nielsen, Shannon M.</creatorcontrib><creatorcontrib>Gibb, James W.</creatorcontrib><creatorcontrib>Alburges, Mario E.</creatorcontrib><creatorcontrib>Wilkins, Diana G.</creatorcontrib><creatorcontrib>Hanson, Glen R.</creatorcontrib><creatorcontrib>Fleckenstein, Annette E.</creatorcontrib><title>Methamphetamine treatment during development attenuates the dopaminergic deficits caused by subsequent high-dose methamphetamine administration</title><title>Synapse (New York, N.Y.)</title><addtitle>Synapse</addtitle><description>Administration of high doses of methamphetamine (METH) causes persistent dopaminergic deficits in both nonhuman preclinical models and METH‐dependent persons. Noteworthy, adolescent [i.e., postnatal day (PND) 40] rats are less susceptible to this damage than young adult (PND90) rats. In addition, biweekly treatment with METH, beginning at PND40 and continuing throughout development, prevents the persistent dopaminergic deficits caused by a “challenge” high‐dose METH regimen when administered at PND90. Mechanisms underlying this “resistance” were thus investigated. Results revealed that biweekly METH treatment throughout development attenuated both the acute and persistent deficits in VMAT2 function, as well as the acute hyperthermia, caused by a challenge METH treatment. Pharmacokinetic alterations did not appear to contribute to the protection afforded by the biweekly treatment. Maintenance of METH‐induced hyperthermia abolished the protection against both the acute and persistent VMAT2‐associated deficits suggesting that alterations in thermoregulation were caused by exposure of rats to METH duringdevelopment. These findings suggest METH during development prevents METH‐induced hyperthermia and the consequent METH‐related neurotoxicity. Synapse 2011. © 2011 Wiley‐Liss, Inc.</description><subject>Adolescence</subject><subject>Animals</subject><subject>Body Temperature Regulation - drug effects</subject><subject>Brain - drug effects</subject><subject>Brain - metabolism</subject><subject>Central Nervous System Stimulants - administration & dosage</subject><subject>Central Nervous System Stimulants - adverse effects</subject><subject>Chromatography, Gas</subject><subject>Development</subject><subject>Dopamine</subject><subject>Dopamine - metabolism</subject><subject>Fever - chemically induced</subject><subject>Growth and Development - drug effects</subject><subject>Hyperthermia</subject><subject>Male</subject><subject>Mass Spectrometry</subject><subject>Methamphetamine</subject><subject>Methamphetamine - administration & dosage</subject><subject>Methamphetamine - adverse effects</subject><subject>Neurotoxicity</subject><subject>Pharmacokinetics</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Synapses</subject><subject>Thermoregulation</subject><subject>Vesicular amine transporter</subject><subject>Vesicular Monoamine Transport Proteins - biosynthesis</subject><subject>vesicular monoamine transporter-2</subject><issn>0887-4476</issn><issn>1098-2396</issn><issn>1098-2396</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kd1u1DAQhS0EokvhghdAuYSLtP6LHd8g0RW0SP1BAoS4srzOZGNI4tR2CvsUvDLubrsCJK5GGn_nzIwPQs8JPiIY0-O4GY8oVpg-QAuCVV1SpsRDtMB1LUvOpThAT2L8hjFmBPPH6IASkmkiF-jXBaTODFMHyQxuhCIFMGmAMRXNHNy4Lhq4gd5P25ZJCcbZJIhF6qBo_LQVhbWzmWuddSkW1swRmmK1KeK8inA93yo7t-7Kxkcohn8GmiYXF1MwyfnxKXrUmj7Cs7t6iD6_e_tpeVaeX52-X745Ly2vK1pWVCgqWsyZFYJY1bBaKoWtoNi0vIGas1yMZJzUHPiqrXKvwlJUikligR2i1zvfaV4N0Ni8YzC9noIbTNhob5z--2V0nV77G80UrhXl2eDlnUHw-cSY9OCihb43I_g5aoKJVEIpQTL6aofa4GMM0O7HEKxvA9Q5QL0NMLMv_txrT94nloHjHfDD9bD5v5P--PXy3rLcKfInw8-9woTvWkgmK_3l8lQzefbhRJ0sNWW_AclFuW4</recordid><startdate>201108</startdate><enddate>201108</enddate><creator>Mcfadden, Lisa M.</creator><creator>Hoonakker, Amanda J.</creator><creator>Vieira-Brock, Paula L.</creator><creator>Stout, Kristen A.</creator><creator>Sawada, Nicole M.</creator><creator>Ellis, Jonathan D.</creator><creator>Allen, Scott C.</creator><creator>Walters, Elliot T.</creator><creator>Nielsen, Shannon M.</creator><creator>Gibb, James W.</creator><creator>Alburges, Mario E.</creator><creator>Wilkins, Diana G.</creator><creator>Hanson, Glen R.</creator><creator>Fleckenstein, Annette E.</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><scope>BSCLL</scope><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>7TK</scope><scope>5PM</scope></search><sort><creationdate>201108</creationdate><title>Methamphetamine treatment during development attenuates the dopaminergic deficits caused by subsequent high-dose methamphetamine administration</title><author>Mcfadden, Lisa M. ; 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Noteworthy, adolescent [i.e., postnatal day (PND) 40] rats are less susceptible to this damage than young adult (PND90) rats. In addition, biweekly treatment with METH, beginning at PND40 and continuing throughout development, prevents the persistent dopaminergic deficits caused by a “challenge” high‐dose METH regimen when administered at PND90. Mechanisms underlying this “resistance” were thus investigated. Results revealed that biweekly METH treatment throughout development attenuated both the acute and persistent deficits in VMAT2 function, as well as the acute hyperthermia, caused by a challenge METH treatment. Pharmacokinetic alterations did not appear to contribute to the protection afforded by the biweekly treatment. Maintenance of METH‐induced hyperthermia abolished the protection against both the acute and persistent VMAT2‐associated deficits suggesting that alterations in thermoregulation were caused by exposure of rats to METH duringdevelopment. These findings suggest METH during development prevents METH‐induced hyperthermia and the consequent METH‐related neurotoxicity. Synapse 2011. © 2011 Wiley‐Liss, Inc.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>21190217</pmid><doi>10.1002/syn.20902</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Wiley Online Library Journals Frontfile Complete |
| subjects | Adolescence Animals Body Temperature Regulation - drug effects Brain - drug effects Brain - metabolism Central Nervous System Stimulants - administration & dosage Central Nervous System Stimulants - adverse effects Chromatography, Gas Development Dopamine Dopamine - metabolism Fever - chemically induced Growth and Development - drug effects Hyperthermia Male Mass Spectrometry Methamphetamine Methamphetamine - administration & dosage Methamphetamine - adverse effects Neurotoxicity Pharmacokinetics Rats Rats, Sprague-Dawley Synapses Thermoregulation Vesicular amine transporter Vesicular Monoamine Transport Proteins - biosynthesis vesicular monoamine transporter-2 |
| title | Methamphetamine treatment during development attenuates the dopaminergic deficits caused by subsequent high-dose methamphetamine administration |
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