2,5-Dimethoxy-4-iodoamphetamine (DOI) Inhibits ∆9-Tetrahydrocannabinol-Induced Catalepsy-Like Immobilization in Mice
∆9-tetrahydrocannabinol, cannabinoid, catalepsy, 2,5-dimethoxy-4-iodoamphetamine (DOI), 5-HT2A receptor
Gespeichert in:
| Autor*in: |
Nobuaki Egashira [verfasserIn] Emi Koushi [verfasserIn] Kenichi Mishima [verfasserIn] Katsunori Iwasaki [verfasserIn] Ryozo Oishi [verfasserIn] Michihiro Fujiwara [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2007 |
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| Übergeordnetes Werk: |
In: Journal of Pharmacological Sciences - Elsevier, 2017, 105(2007), 4, Seite 361-366 |
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| Übergeordnetes Werk: |
volume:105 ; year:2007 ; number:4 ; pages:361-366 |
| Links: |
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| DOI / URN: |
10.1254/jphs.FP0071247 |
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| Katalog-ID: |
DOAJ049773895 |
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| 520 | |a The effect of the serotonin 5-HT2A/2C-receptor agonist 2,5-dimethoxy-4-iodoamphetamine (DOI) on ∆9-tetrahydrocannabinol (THC)-induced catalepsy-like immobilization was studied in mice. DOI (0.3 and 1 mg/kg, i.p.) significantly inhibited the catalepsy-like immobilization induced by THC (10 mg/kg, i.p.). In contrast, the selective 5-HT2C-receptor agonist 8,9-dichloro-2,3,4,4a-tetrahydro-1H-pyrazino[1,2-a]quinoxalin-5(6H)-one (WAY 161503) had no effect on this catalepsy-like immobilization. Moreover, the 5-HT2A-receptor antagonist ketanserin (0.3 mg/kg, i.p.) reversed the inhibition of THC-induced catalepsy-like immobilization caused by DOI (1 mg/kg), whereas the selective 5-HT2C-receptor antagonist 6-chloro-2,3-dihydro-5-methyl-N-[6-(2-methyl-3-pyridinyl)oxyl]-3-pyridinyl]-1H-indole-1-carboxyamide (SB 242084) did not affect this inhibitory effect of DOI. On the other hand, ketanserin (0.3 and 1 mg/kg, i.p.) enhanced the catalepsy-like immobilization induced by THC (6 mg/kg, i.p.). Thus, on the basis of these results, it appears that 5-HT2A-receptor mechanisms might be responsible for the inhibitory effect of DOI on THC-induced catalepsy-like immobilization. Keywords:: ∆9-tetrahydrocannabinol, cannabinoid, catalepsy, 2,5-dimethoxy-4-iodoamphetamine (DOI), 5-HT2A receptor | ||
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10.1254/jphs.FP0071247 doi (DE-627)DOAJ049773895 (DE-599)DOAJ026460ac577c40e8b515b64cb15fbc23 DE-627 ger DE-627 rakwb eng RM1-950 Nobuaki Egashira verfasserin aut 2,5-Dimethoxy-4-iodoamphetamine (DOI) Inhibits ∆9-Tetrahydrocannabinol-Induced Catalepsy-Like Immobilization in Mice 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The effect of the serotonin 5-HT2A/2C-receptor agonist 2,5-dimethoxy-4-iodoamphetamine (DOI) on ∆9-tetrahydrocannabinol (THC)-induced catalepsy-like immobilization was studied in mice. DOI (0.3 and 1 mg/kg, i.p.) significantly inhibited the catalepsy-like immobilization induced by THC (10 mg/kg, i.p.). In contrast, the selective 5-HT2C-receptor agonist 8,9-dichloro-2,3,4,4a-tetrahydro-1H-pyrazino[1,2-a]quinoxalin-5(6H)-one (WAY 161503) had no effect on this catalepsy-like immobilization. Moreover, the 5-HT2A-receptor antagonist ketanserin (0.3 mg/kg, i.p.) reversed the inhibition of THC-induced catalepsy-like immobilization caused by DOI (1 mg/kg), whereas the selective 5-HT2C-receptor antagonist 6-chloro-2,3-dihydro-5-methyl-N-[6-(2-methyl-3-pyridinyl)oxyl]-3-pyridinyl]-1H-indole-1-carboxyamide (SB 242084) did not affect this inhibitory effect of DOI. On the other hand, ketanserin (0.3 and 1 mg/kg, i.p.) enhanced the catalepsy-like immobilization induced by THC (6 mg/kg, i.p.). Thus, on the basis of these results, it appears that 5-HT2A-receptor mechanisms might be responsible for the inhibitory effect of DOI on THC-induced catalepsy-like immobilization. Keywords:: ∆9-tetrahydrocannabinol, cannabinoid, catalepsy, 2,5-dimethoxy-4-iodoamphetamine (DOI), 5-HT2A receptor Therapeutics. Pharmacology Emi Koushi verfasserin aut Kenichi Mishima verfasserin aut Katsunori Iwasaki verfasserin aut Ryozo Oishi verfasserin aut Michihiro Fujiwara verfasserin aut In Journal of Pharmacological Sciences Elsevier, 2017 105(2007), 4, Seite 361-366 (DE-627)1760631620 13478613 nnns volume:105 year:2007 number:4 pages:361-366 https://doi.org/10.1254/jphs.FP0071247 kostenfrei https://doaj.org/article/026460ac577c40e8b515b64cb15fbc23 kostenfrei http://www.sciencedirect.com/science/article/pii/S1347861319341829 kostenfrei https://doaj.org/toc/1347-8613 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ AR 105 2007 4 361-366 |
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10.1254/jphs.FP0071247 doi (DE-627)DOAJ049773895 (DE-599)DOAJ026460ac577c40e8b515b64cb15fbc23 DE-627 ger DE-627 rakwb eng RM1-950 Nobuaki Egashira verfasserin aut 2,5-Dimethoxy-4-iodoamphetamine (DOI) Inhibits ∆9-Tetrahydrocannabinol-Induced Catalepsy-Like Immobilization in Mice 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The effect of the serotonin 5-HT2A/2C-receptor agonist 2,5-dimethoxy-4-iodoamphetamine (DOI) on ∆9-tetrahydrocannabinol (THC)-induced catalepsy-like immobilization was studied in mice. DOI (0.3 and 1 mg/kg, i.p.) significantly inhibited the catalepsy-like immobilization induced by THC (10 mg/kg, i.p.). In contrast, the selective 5-HT2C-receptor agonist 8,9-dichloro-2,3,4,4a-tetrahydro-1H-pyrazino[1,2-a]quinoxalin-5(6H)-one (WAY 161503) had no effect on this catalepsy-like immobilization. Moreover, the 5-HT2A-receptor antagonist ketanserin (0.3 mg/kg, i.p.) reversed the inhibition of THC-induced catalepsy-like immobilization caused by DOI (1 mg/kg), whereas the selective 5-HT2C-receptor antagonist 6-chloro-2,3-dihydro-5-methyl-N-[6-(2-methyl-3-pyridinyl)oxyl]-3-pyridinyl]-1H-indole-1-carboxyamide (SB 242084) did not affect this inhibitory effect of DOI. On the other hand, ketanserin (0.3 and 1 mg/kg, i.p.) enhanced the catalepsy-like immobilization induced by THC (6 mg/kg, i.p.). Thus, on the basis of these results, it appears that 5-HT2A-receptor mechanisms might be responsible for the inhibitory effect of DOI on THC-induced catalepsy-like immobilization. Keywords:: ∆9-tetrahydrocannabinol, cannabinoid, catalepsy, 2,5-dimethoxy-4-iodoamphetamine (DOI), 5-HT2A receptor Therapeutics. Pharmacology Emi Koushi verfasserin aut Kenichi Mishima verfasserin aut Katsunori Iwasaki verfasserin aut Ryozo Oishi verfasserin aut Michihiro Fujiwara verfasserin aut In Journal of Pharmacological Sciences Elsevier, 2017 105(2007), 4, Seite 361-366 (DE-627)1760631620 13478613 nnns volume:105 year:2007 number:4 pages:361-366 https://doi.org/10.1254/jphs.FP0071247 kostenfrei https://doaj.org/article/026460ac577c40e8b515b64cb15fbc23 kostenfrei http://www.sciencedirect.com/science/article/pii/S1347861319341829 kostenfrei https://doaj.org/toc/1347-8613 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ AR 105 2007 4 361-366 |
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10.1254/jphs.FP0071247 doi (DE-627)DOAJ049773895 (DE-599)DOAJ026460ac577c40e8b515b64cb15fbc23 DE-627 ger DE-627 rakwb eng RM1-950 Nobuaki Egashira verfasserin aut 2,5-Dimethoxy-4-iodoamphetamine (DOI) Inhibits ∆9-Tetrahydrocannabinol-Induced Catalepsy-Like Immobilization in Mice 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The effect of the serotonin 5-HT2A/2C-receptor agonist 2,5-dimethoxy-4-iodoamphetamine (DOI) on ∆9-tetrahydrocannabinol (THC)-induced catalepsy-like immobilization was studied in mice. DOI (0.3 and 1 mg/kg, i.p.) significantly inhibited the catalepsy-like immobilization induced by THC (10 mg/kg, i.p.). In contrast, the selective 5-HT2C-receptor agonist 8,9-dichloro-2,3,4,4a-tetrahydro-1H-pyrazino[1,2-a]quinoxalin-5(6H)-one (WAY 161503) had no effect on this catalepsy-like immobilization. Moreover, the 5-HT2A-receptor antagonist ketanserin (0.3 mg/kg, i.p.) reversed the inhibition of THC-induced catalepsy-like immobilization caused by DOI (1 mg/kg), whereas the selective 5-HT2C-receptor antagonist 6-chloro-2,3-dihydro-5-methyl-N-[6-(2-methyl-3-pyridinyl)oxyl]-3-pyridinyl]-1H-indole-1-carboxyamide (SB 242084) did not affect this inhibitory effect of DOI. On the other hand, ketanserin (0.3 and 1 mg/kg, i.p.) enhanced the catalepsy-like immobilization induced by THC (6 mg/kg, i.p.). Thus, on the basis of these results, it appears that 5-HT2A-receptor mechanisms might be responsible for the inhibitory effect of DOI on THC-induced catalepsy-like immobilization. Keywords:: ∆9-tetrahydrocannabinol, cannabinoid, catalepsy, 2,5-dimethoxy-4-iodoamphetamine (DOI), 5-HT2A receptor Therapeutics. Pharmacology Emi Koushi verfasserin aut Kenichi Mishima verfasserin aut Katsunori Iwasaki verfasserin aut Ryozo Oishi verfasserin aut Michihiro Fujiwara verfasserin aut In Journal of Pharmacological Sciences Elsevier, 2017 105(2007), 4, Seite 361-366 (DE-627)1760631620 13478613 nnns volume:105 year:2007 number:4 pages:361-366 https://doi.org/10.1254/jphs.FP0071247 kostenfrei https://doaj.org/article/026460ac577c40e8b515b64cb15fbc23 kostenfrei http://www.sciencedirect.com/science/article/pii/S1347861319341829 kostenfrei https://doaj.org/toc/1347-8613 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ AR 105 2007 4 361-366 |
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10.1254/jphs.FP0071247 doi (DE-627)DOAJ049773895 (DE-599)DOAJ026460ac577c40e8b515b64cb15fbc23 DE-627 ger DE-627 rakwb eng RM1-950 Nobuaki Egashira verfasserin aut 2,5-Dimethoxy-4-iodoamphetamine (DOI) Inhibits ∆9-Tetrahydrocannabinol-Induced Catalepsy-Like Immobilization in Mice 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The effect of the serotonin 5-HT2A/2C-receptor agonist 2,5-dimethoxy-4-iodoamphetamine (DOI) on ∆9-tetrahydrocannabinol (THC)-induced catalepsy-like immobilization was studied in mice. DOI (0.3 and 1 mg/kg, i.p.) significantly inhibited the catalepsy-like immobilization induced by THC (10 mg/kg, i.p.). In contrast, the selective 5-HT2C-receptor agonist 8,9-dichloro-2,3,4,4a-tetrahydro-1H-pyrazino[1,2-a]quinoxalin-5(6H)-one (WAY 161503) had no effect on this catalepsy-like immobilization. Moreover, the 5-HT2A-receptor antagonist ketanserin (0.3 mg/kg, i.p.) reversed the inhibition of THC-induced catalepsy-like immobilization caused by DOI (1 mg/kg), whereas the selective 5-HT2C-receptor antagonist 6-chloro-2,3-dihydro-5-methyl-N-[6-(2-methyl-3-pyridinyl)oxyl]-3-pyridinyl]-1H-indole-1-carboxyamide (SB 242084) did not affect this inhibitory effect of DOI. On the other hand, ketanserin (0.3 and 1 mg/kg, i.p.) enhanced the catalepsy-like immobilization induced by THC (6 mg/kg, i.p.). Thus, on the basis of these results, it appears that 5-HT2A-receptor mechanisms might be responsible for the inhibitory effect of DOI on THC-induced catalepsy-like immobilization. Keywords:: ∆9-tetrahydrocannabinol, cannabinoid, catalepsy, 2,5-dimethoxy-4-iodoamphetamine (DOI), 5-HT2A receptor Therapeutics. Pharmacology Emi Koushi verfasserin aut Kenichi Mishima verfasserin aut Katsunori Iwasaki verfasserin aut Ryozo Oishi verfasserin aut Michihiro Fujiwara verfasserin aut In Journal of Pharmacological Sciences Elsevier, 2017 105(2007), 4, Seite 361-366 (DE-627)1760631620 13478613 nnns volume:105 year:2007 number:4 pages:361-366 https://doi.org/10.1254/jphs.FP0071247 kostenfrei https://doaj.org/article/026460ac577c40e8b515b64cb15fbc23 kostenfrei http://www.sciencedirect.com/science/article/pii/S1347861319341829 kostenfrei https://doaj.org/toc/1347-8613 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ AR 105 2007 4 361-366 |
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10.1254/jphs.FP0071247 doi (DE-627)DOAJ049773895 (DE-599)DOAJ026460ac577c40e8b515b64cb15fbc23 DE-627 ger DE-627 rakwb eng RM1-950 Nobuaki Egashira verfasserin aut 2,5-Dimethoxy-4-iodoamphetamine (DOI) Inhibits ∆9-Tetrahydrocannabinol-Induced Catalepsy-Like Immobilization in Mice 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The effect of the serotonin 5-HT2A/2C-receptor agonist 2,5-dimethoxy-4-iodoamphetamine (DOI) on ∆9-tetrahydrocannabinol (THC)-induced catalepsy-like immobilization was studied in mice. DOI (0.3 and 1 mg/kg, i.p.) significantly inhibited the catalepsy-like immobilization induced by THC (10 mg/kg, i.p.). In contrast, the selective 5-HT2C-receptor agonist 8,9-dichloro-2,3,4,4a-tetrahydro-1H-pyrazino[1,2-a]quinoxalin-5(6H)-one (WAY 161503) had no effect on this catalepsy-like immobilization. Moreover, the 5-HT2A-receptor antagonist ketanserin (0.3 mg/kg, i.p.) reversed the inhibition of THC-induced catalepsy-like immobilization caused by DOI (1 mg/kg), whereas the selective 5-HT2C-receptor antagonist 6-chloro-2,3-dihydro-5-methyl-N-[6-(2-methyl-3-pyridinyl)oxyl]-3-pyridinyl]-1H-indole-1-carboxyamide (SB 242084) did not affect this inhibitory effect of DOI. On the other hand, ketanserin (0.3 and 1 mg/kg, i.p.) enhanced the catalepsy-like immobilization induced by THC (6 mg/kg, i.p.). Thus, on the basis of these results, it appears that 5-HT2A-receptor mechanisms might be responsible for the inhibitory effect of DOI on THC-induced catalepsy-like immobilization. Keywords:: ∆9-tetrahydrocannabinol, cannabinoid, catalepsy, 2,5-dimethoxy-4-iodoamphetamine (DOI), 5-HT2A receptor Therapeutics. Pharmacology Emi Koushi verfasserin aut Kenichi Mishima verfasserin aut Katsunori Iwasaki verfasserin aut Ryozo Oishi verfasserin aut Michihiro Fujiwara verfasserin aut In Journal of Pharmacological Sciences Elsevier, 2017 105(2007), 4, Seite 361-366 (DE-627)1760631620 13478613 nnns volume:105 year:2007 number:4 pages:361-366 https://doi.org/10.1254/jphs.FP0071247 kostenfrei https://doaj.org/article/026460ac577c40e8b515b64cb15fbc23 kostenfrei http://www.sciencedirect.com/science/article/pii/S1347861319341829 kostenfrei https://doaj.org/toc/1347-8613 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ AR 105 2007 4 361-366 |
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DOI (0.3 and 1 mg/kg, i.p.) significantly inhibited the catalepsy-like immobilization induced by THC (10 mg/kg, i.p.). In contrast, the selective 5-HT2C-receptor agonist 8,9-dichloro-2,3,4,4a-tetrahydro-1H-pyrazino[1,2-a]quinoxalin-5(6H)-one (WAY 161503) had no effect on this catalepsy-like immobilization. Moreover, the 5-HT2A-receptor antagonist ketanserin (0.3 mg/kg, i.p.) reversed the inhibition of THC-induced catalepsy-like immobilization caused by DOI (1 mg/kg), whereas the selective 5-HT2C-receptor antagonist 6-chloro-2,3-dihydro-5-methyl-N-[6-(2-methyl-3-pyridinyl)oxyl]-3-pyridinyl]-1H-indole-1-carboxyamide (SB 242084) did not affect this inhibitory effect of DOI. On the other hand, ketanserin (0.3 and 1 mg/kg, i.p.) enhanced the catalepsy-like immobilization induced by THC (6 mg/kg, i.p.). Thus, on the basis of these results, it appears that 5-HT2A-receptor mechanisms might be responsible for the inhibitory effect of DOI on THC-induced catalepsy-like immobilization. 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2,5-dimethoxy-4-iodoamphetamine (doi) inhibits ∆9-tetrahydrocannabinol-induced catalepsy-like immobilization in mice |
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2,5-Dimethoxy-4-iodoamphetamine (DOI) Inhibits ∆9-Tetrahydrocannabinol-Induced Catalepsy-Like Immobilization in Mice |
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The effect of the serotonin 5-HT2A/2C-receptor agonist 2,5-dimethoxy-4-iodoamphetamine (DOI) on ∆9-tetrahydrocannabinol (THC)-induced catalepsy-like immobilization was studied in mice. DOI (0.3 and 1 mg/kg, i.p.) significantly inhibited the catalepsy-like immobilization induced by THC (10 mg/kg, i.p.). In contrast, the selective 5-HT2C-receptor agonist 8,9-dichloro-2,3,4,4a-tetrahydro-1H-pyrazino[1,2-a]quinoxalin-5(6H)-one (WAY 161503) had no effect on this catalepsy-like immobilization. Moreover, the 5-HT2A-receptor antagonist ketanserin (0.3 mg/kg, i.p.) reversed the inhibition of THC-induced catalepsy-like immobilization caused by DOI (1 mg/kg), whereas the selective 5-HT2C-receptor antagonist 6-chloro-2,3-dihydro-5-methyl-N-[6-(2-methyl-3-pyridinyl)oxyl]-3-pyridinyl]-1H-indole-1-carboxyamide (SB 242084) did not affect this inhibitory effect of DOI. On the other hand, ketanserin (0.3 and 1 mg/kg, i.p.) enhanced the catalepsy-like immobilization induced by THC (6 mg/kg, i.p.). Thus, on the basis of these results, it appears that 5-HT2A-receptor mechanisms might be responsible for the inhibitory effect of DOI on THC-induced catalepsy-like immobilization. Keywords:: ∆9-tetrahydrocannabinol, cannabinoid, catalepsy, 2,5-dimethoxy-4-iodoamphetamine (DOI), 5-HT2A receptor |
| abstractGer |
The effect of the serotonin 5-HT2A/2C-receptor agonist 2,5-dimethoxy-4-iodoamphetamine (DOI) on ∆9-tetrahydrocannabinol (THC)-induced catalepsy-like immobilization was studied in mice. DOI (0.3 and 1 mg/kg, i.p.) significantly inhibited the catalepsy-like immobilization induced by THC (10 mg/kg, i.p.). In contrast, the selective 5-HT2C-receptor agonist 8,9-dichloro-2,3,4,4a-tetrahydro-1H-pyrazino[1,2-a]quinoxalin-5(6H)-one (WAY 161503) had no effect on this catalepsy-like immobilization. Moreover, the 5-HT2A-receptor antagonist ketanserin (0.3 mg/kg, i.p.) reversed the inhibition of THC-induced catalepsy-like immobilization caused by DOI (1 mg/kg), whereas the selective 5-HT2C-receptor antagonist 6-chloro-2,3-dihydro-5-methyl-N-[6-(2-methyl-3-pyridinyl)oxyl]-3-pyridinyl]-1H-indole-1-carboxyamide (SB 242084) did not affect this inhibitory effect of DOI. On the other hand, ketanserin (0.3 and 1 mg/kg, i.p.) enhanced the catalepsy-like immobilization induced by THC (6 mg/kg, i.p.). Thus, on the basis of these results, it appears that 5-HT2A-receptor mechanisms might be responsible for the inhibitory effect of DOI on THC-induced catalepsy-like immobilization. Keywords:: ∆9-tetrahydrocannabinol, cannabinoid, catalepsy, 2,5-dimethoxy-4-iodoamphetamine (DOI), 5-HT2A receptor |
| abstract_unstemmed |
The effect of the serotonin 5-HT2A/2C-receptor agonist 2,5-dimethoxy-4-iodoamphetamine (DOI) on ∆9-tetrahydrocannabinol (THC)-induced catalepsy-like immobilization was studied in mice. DOI (0.3 and 1 mg/kg, i.p.) significantly inhibited the catalepsy-like immobilization induced by THC (10 mg/kg, i.p.). In contrast, the selective 5-HT2C-receptor agonist 8,9-dichloro-2,3,4,4a-tetrahydro-1H-pyrazino[1,2-a]quinoxalin-5(6H)-one (WAY 161503) had no effect on this catalepsy-like immobilization. Moreover, the 5-HT2A-receptor antagonist ketanserin (0.3 mg/kg, i.p.) reversed the inhibition of THC-induced catalepsy-like immobilization caused by DOI (1 mg/kg), whereas the selective 5-HT2C-receptor antagonist 6-chloro-2,3-dihydro-5-methyl-N-[6-(2-methyl-3-pyridinyl)oxyl]-3-pyridinyl]-1H-indole-1-carboxyamide (SB 242084) did not affect this inhibitory effect of DOI. On the other hand, ketanserin (0.3 and 1 mg/kg, i.p.) enhanced the catalepsy-like immobilization induced by THC (6 mg/kg, i.p.). Thus, on the basis of these results, it appears that 5-HT2A-receptor mechanisms might be responsible for the inhibitory effect of DOI on THC-induced catalepsy-like immobilization. Keywords:: ∆9-tetrahydrocannabinol, cannabinoid, catalepsy, 2,5-dimethoxy-4-iodoamphetamine (DOI), 5-HT2A receptor |
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