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題名 The group II metabotropic glutamate receptor agonist LY379268 reduces toluene-induced enhancement of brain-stimulation reward and behavioral disturbances
作者 Chan, Ming-Huan;Tsai, Yi-Ling;Lee, Mei-Yi;Stoker, Astrid;Markou, K. Athina;Chen, Hwei-Hsien
詹銘煥;蔡依玲
貢獻者 神經科學研究所;心腦學研究中心
關鍵詞 Toluene;mGluR2/3;Motor coordination;Object recognition;Social interaction;Intracranial self-stimulation
日期 2015-06
上傳時間 5-Aug-2015 14:11:45 (UTC+8)
摘要 Rationale Toluene, a widely abused solvent with demonstrated addictive potential in humans, hasbeen reported to negatively modulate N-methyl-D-aspartate receptors (NMDARs) and alter glutamatergicneurotransmission. The group II metabotropic glutamate receptor (mGluR) agonist LY379268 has beenshown to regulate glutamate release transmission and NMDAR function and block toluene-induced locomotorhyperactivity. However, remaining unknown is whether group II mGluRs are involved in the toluene-induced reward-facilitating effect and other behavioral manifestations. Objectives The present study evaluated the effects of LY379268 on toluene-induced reward enhancement, motor incoordination, recognition memory impairment, and social interaction deficits. Results Our data demonstrated that LY379268 significantly reversed the toluene-induced lowering of intracranial selfstimulation (ICSS) thresholds and impairments in novel objectrecognition, rotarod performance, and social interaction with different potencies. Conclusions These results indicate a negative modulatory role of group II mGluRs in acute toluene-induced reward-facilitating and behavioral effects and suggest that group II mGluR agonists may have therapeutic potential for toluene addiction and the prevention of toluene intoxication caused by occupational or intentional exposure.
關聯 Psychopharmacology
資料類型 article
DOI http://dx.doi.org/10.1007/s00213-015-3973-3
dc.contributor 神經科學研究所;心腦學研究中心-
dc.creator (作者) Chan, Ming-Huan;Tsai, Yi-Ling;Lee, Mei-Yi;Stoker, Astrid;Markou, K. Athina;Chen, Hwei-Hsien-
dc.creator (作者) 詹銘煥;蔡依玲-
dc.date (日期) 2015-06-
dc.date.accessioned 5-Aug-2015 14:11:45 (UTC+8)-
dc.date.available 5-Aug-2015 14:11:45 (UTC+8)-
dc.date.issued (上傳時間) 5-Aug-2015 14:11:45 (UTC+8)-
dc.identifier.uri (URI) http://nccur.lib.nccu.edu.tw/handle/140.119/77409-
dc.description.abstract (摘要) Rationale Toluene, a widely abused solvent with demonstrated addictive potential in humans, hasbeen reported to negatively modulate N-methyl-D-aspartate receptors (NMDARs) and alter glutamatergicneurotransmission. The group II metabotropic glutamate receptor (mGluR) agonist LY379268 has beenshown to regulate glutamate release transmission and NMDAR function and block toluene-induced locomotorhyperactivity. However, remaining unknown is whether group II mGluRs are involved in the toluene-induced reward-facilitating effect and other behavioral manifestations. Objectives The present study evaluated the effects of LY379268 on toluene-induced reward enhancement, motor incoordination, recognition memory impairment, and social interaction deficits. Results Our data demonstrated that LY379268 significantly reversed the toluene-induced lowering of intracranial selfstimulation (ICSS) thresholds and impairments in novel objectrecognition, rotarod performance, and social interaction with different potencies. Conclusions These results indicate a negative modulatory role of group II mGluRs in acute toluene-induced reward-facilitating and behavioral effects and suggest that group II mGluR agonists may have therapeutic potential for toluene addiction and the prevention of toluene intoxication caused by occupational or intentional exposure.-
dc.format.extent 935049 bytes-
dc.format.mimetype application/pdf-
dc.relation (關聯) Psychopharmacology-
dc.subject (關鍵詞) Toluene;mGluR2/3;Motor coordination;Object recognition;Social interaction;Intracranial self-stimulation-
dc.title (題名) The group II metabotropic glutamate receptor agonist LY379268 reduces toluene-induced enhancement of brain-stimulation reward and behavioral disturbances-
dc.type (資料類型) articleen
dc.identifier.doi (DOI) 10.1007/s00213-015-3973-3-
dc.doi.uri (DOI) http://dx.doi.org/10.1007/s00213-015-3973-3-