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(1-(2,5-dimethoxy-4 iodophenyl)-2-aminopropane)-induced head-twitches in the rat are mediated by 5-hydroxytryptamine (5-HT) 2A receptors: modulation by novel 5-HT2A/2C antagonists, D1 antagonists and 5-HT1A agonists.
J Pharmacol Exp Ther. 1995 Apr; 273(1):101-12.JP

Abstract

In this study, the involvement of serotonergic and dopaminergic receptors in the modulation of the head-twitch (HTW) response to the 5-hydroxytryptamine (5-HT)2A/5-HT2C agonist, 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane, was characterized in rats using novel and selective ligands at 5-HT2A, 5-HT2C, D1, D2 and 5-HT1A receptors. HTW were dose-dependently inhibited by the 5-HT2A/2C antagonists, ritanserin, metergoline, mesulergine, mianserin, ICI 169,369 and LY 58,537, by the preferential 5-HT2A antagonist, ketanserin and by the novel, selective 5-HT2A antagonist, SR 46349B. A further selective 5-HT2A antagonist, MDL 100,907, very potently abolished HTW (ED50 = 0.005 mg/kg). The order of relative potency correlated highly with their affinity at 5-HT2A (r = 0.83) but not 5-HT2C receptors (r = 0.06). In addition, the novel, selective 5-HT2C antagonist, SB 200,646A, failed to abolish HTW and the 5-HT2C agonists/5-HT2A antagonists, 1-(3-chlorophenyl)piperazine and 1-(3-trifluoromethylphenyl)piperazine, blocked, rather than elicited, HTW. The D1 antagonists, SCH 23390, NNC 112, NNC 756, SCH 39166 and A 69024, in this order of relative potency that correlated with their affinity at D1 receptors (r = 0.98), blocked HTW. The D2 antagonists, raclopride, eticlopride and haloperidol also blocked HTW. The 5-HT1A agonists, S 14671, S 14506, 8-hydroxy-2-(di-n-propylamino)tetralin, buspirone, ipsapirone and (+)-flesinoxan, abolished HTW. The action of 8-hydroxy-2-(di-n-propylamino)tetralin was blocked by (-)-tertatolol (ID50 = 4.5 mg/kg), a novel 5-HT1A receptor antagonist. Similarly, (-)-tertatolol attenuated the action of S 14506 and abolished that of S 14671, buspirone and ipsapirone. A role of postsynaptic 5-HT1A receptors in the action of 5-HT1A agonists was suggested by the finding that parachlorophenylalanine (3 x 300 mg/kg, i.p.), which depleted cerebral pools of 5-HT, did not modify the activity of ipsapirone. The present data demonstrate that 5-HT2A receptors mediate HTW in rats and that both D1 and D2 receptors as well as (postsynaptic) 5-HT1A receptors play a role in their expression.

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Authors+Show Affiliations

Schreiber R
Department of Psychopharmacology, Centre de Recherches Croissy, Croissy-sur-Seine, France.
Brocco M
No affiliation info available
Audinot V
No affiliation info available
Gobert A
No affiliation info available
Veiga S
No affiliation info available
Millan MJ
No affiliation info available

MeSH

8-Hydroxy-2-(di-n-propylamino)tetralinAmphetaminesAnimalsBehavior, AnimalBenzazepinesDopamine AntagonistsMalePiperazinesQuipazineRatsRats, WistarReceptors, AdrenergicReceptors, Dopamine D1Receptors, SerotoninSerotonin AntagonistsSerotonin Receptor Agonists

Pub Type(s)

Journal Article

Language

eng

PubMed ID

7714755

Citation

Schreiber, R, et al. "(1-(2,5-dimethoxy-4 Iodophenyl)-2-aminopropane)-induced Head-twitches in the Rat Are Mediated By 5-hydroxytryptamine (5-HT) 2A Receptors: Modulation By Novel 5-HT2A/2C Antagonists, D1 Antagonists and 5-HT1A Agonists." The Journal of Pharmacology and Experimental Therapeutics, vol. 273, no. 1, 1995, pp. 101-12.
Schreiber R, Brocco M, Audinot V, et al. (1-(2,5-dimethoxy-4 iodophenyl)-2-aminopropane)-induced head-twitches in the rat are mediated by 5-hydroxytryptamine (5-HT) 2A receptors: modulation by novel 5-HT2A/2C antagonists, D1 antagonists and 5-HT1A agonists. J Pharmacol Exp Ther. 1995;273(1):101-12.
Schreiber, R., Brocco, M., Audinot, V., Gobert, A., Veiga, S., & Millan, M. J. (1995). (1-(2,5-dimethoxy-4 iodophenyl)-2-aminopropane)-induced head-twitches in the rat are mediated by 5-hydroxytryptamine (5-HT) 2A receptors: modulation by novel 5-HT2A/2C antagonists, D1 antagonists and 5-HT1A agonists. The Journal of Pharmacology and Experimental Therapeutics, 273(1), 101-12.
Schreiber R, et al. (1-(2,5-dimethoxy-4 Iodophenyl)-2-aminopropane)-induced Head-twitches in the Rat Are Mediated By 5-hydroxytryptamine (5-HT) 2A Receptors: Modulation By Novel 5-HT2A/2C Antagonists, D1 Antagonists and 5-HT1A Agonists. J Pharmacol Exp Ther. 1995;273(1):101-12. PubMed PMID: 7714755.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - (1-(2,5-dimethoxy-4 iodophenyl)-2-aminopropane)-induced head-twitches in the rat are mediated by 5-hydroxytryptamine (5-HT) 2A receptors: modulation by novel 5-HT2A/2C antagonists, D1 antagonists and 5-HT1A agonists. AU - Schreiber,R, AU - Brocco,M, AU - Audinot,V, AU - Gobert,A, AU - Veiga,S, AU - Millan,M J, PY - 1995/4/1/pubmed PY - 1995/4/1/medline PY - 1995/4/1/entrez SP - 101 EP - 12 JF - The Journal of pharmacology and experimental therapeutics JO - J Pharmacol Exp Ther VL - 273 IS - 1 N2 - In this study, the involvement of serotonergic and dopaminergic receptors in the modulation of the head-twitch (HTW) response to the 5-hydroxytryptamine (5-HT)2A/5-HT2C agonist, 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane, was characterized in rats using novel and selective ligands at 5-HT2A, 5-HT2C, D1, D2 and 5-HT1A receptors. HTW were dose-dependently inhibited by the 5-HT2A/2C antagonists, ritanserin, metergoline, mesulergine, mianserin, ICI 169,369 and LY 58,537, by the preferential 5-HT2A antagonist, ketanserin and by the novel, selective 5-HT2A antagonist, SR 46349B. A further selective 5-HT2A antagonist, MDL 100,907, very potently abolished HTW (ED50 = 0.005 mg/kg). The order of relative potency correlated highly with their affinity at 5-HT2A (r = 0.83) but not 5-HT2C receptors (r = 0.06). In addition, the novel, selective 5-HT2C antagonist, SB 200,646A, failed to abolish HTW and the 5-HT2C agonists/5-HT2A antagonists, 1-(3-chlorophenyl)piperazine and 1-(3-trifluoromethylphenyl)piperazine, blocked, rather than elicited, HTW. The D1 antagonists, SCH 23390, NNC 112, NNC 756, SCH 39166 and A 69024, in this order of relative potency that correlated with their affinity at D1 receptors (r = 0.98), blocked HTW. The D2 antagonists, raclopride, eticlopride and haloperidol also blocked HTW. The 5-HT1A agonists, S 14671, S 14506, 8-hydroxy-2-(di-n-propylamino)tetralin, buspirone, ipsapirone and (+)-flesinoxan, abolished HTW. The action of 8-hydroxy-2-(di-n-propylamino)tetralin was blocked by (-)-tertatolol (ID50 = 4.5 mg/kg), a novel 5-HT1A receptor antagonist. Similarly, (-)-tertatolol attenuated the action of S 14506 and abolished that of S 14671, buspirone and ipsapirone. A role of postsynaptic 5-HT1A receptors in the action of 5-HT1A agonists was suggested by the finding that parachlorophenylalanine (3 x 300 mg/kg, i.p.), which depleted cerebral pools of 5-HT, did not modify the activity of ipsapirone. The present data demonstrate that 5-HT2A receptors mediate HTW in rats and that both D1 and D2 receptors as well as (postsynaptic) 5-HT1A receptors play a role in their expression. SN - 0022-3565 UR - https://www.unboundmedicine.com/medline/citation/7714755/_1__25_dimethoxy_4_iodophenyl__2_aminopropane__induced_head_twitches_in_the_rat_are_mediated_by_5_hydroxytryptamine__5_HT__2A_receptors:_modulation_by_novel_5_HT2A/2C_antagonists_D1_antagonists_and_5_HT1A_agonists_ L2 - https://jpet.aspetjournals.org/cgi/pmidlookup?view=long&pmid=7714755 DB - PRIME DP - Unbound Medicine ER -