8-Hydroxy-2-(Di-n-propylamino)tetralin (8-OH-DPAT) elicits eating in free-feeding rats by acting on central serotonin neurons

C. Bendotti; R. Samanin

doi:10.1016/0014-2999(86)90405-X

8-Hydroxy-2-(Di-n-propylamino)tetralin (8-OH-DPAT) elicits eating in free-feeding rats by acting on central serotonin neurons

C. Bendotti, R. Samanin

Istituto di Ricerche Farmacologiche "Mario Negri"

Research output: Contribution to journal › Article

Abstract

A subcutaneous injection of 0.5 mg/kg 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), a drug with high affinity for 5-hydroxytryptamine (5-HT_1A) binding sites, substantially increased eating in non-deprived rats. Intraventricular injections of 5,7-dihydroxytryptamine (5,7-DHT), a neurotoxin for 5-HT neurons, also significantly increased eating in rats and antagonized the effect of 8-OH-DPAT. Microinjections of 8-OH-DPAT (0.5 and 1 μg) in the nuclei dorsalis and medianus raphe also significantly increased eating in rats. 8-OH-DPAT appears to stimulate eating by acting on 5-HT-containing neurons. These results are compatible wwith the hypothesis that a decrease in central 5-HT function disinhibits feeding.

Original language	English
Pages (from-to)	147-150
Number of pages	4
Journal	European Journal of Pharmacology
Volume	121
Issue number	1
DOIs	https://doi.org/10.1016/0014-2999(86)90405-X
Publication status	Published - Feb 11 1986

Keywords

8-Hydroxy-2-(di-n-propylamino)tetralin
Feeding
Serotonin receptors

ASJC Scopus subject areas

Cellular and Molecular Neuroscience
Pharmacology

Access to Document

10.1016/0014-2999(86)90405-X

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Bendotti, C., & Samanin, R. (1986). 8-Hydroxy-2-(Di-n-propylamino)tetralin (8-OH-DPAT) elicits eating in free-feeding rats by acting on central serotonin neurons. European Journal of Pharmacology, 121(1), 147-150. https://doi.org/10.1016/0014-2999(86)90405-X

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title = "8-Hydroxy-2-(Di-n-propylamino)tetralin (8-OH-DPAT) elicits eating in free-feeding rats by acting on central serotonin neurons",

abstract = "A subcutaneous injection of 0.5 mg/kg 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), a drug with high affinity for 5-hydroxytryptamine (5-HT1A) binding sites, substantially increased eating in non-deprived rats. Intraventricular injections of 5,7-dihydroxytryptamine (5,7-DHT), a neurotoxin for 5-HT neurons, also significantly increased eating in rats and antagonized the effect of 8-OH-DPAT. Microinjections of 8-OH-DPAT (0.5 and 1 μg) in the nuclei dorsalis and medianus raphe also significantly increased eating in rats. 8-OH-DPAT appears to stimulate eating by acting on 5-HT-containing neurons. These results are compatible wwith the hypothesis that a decrease in central 5-HT function disinhibits feeding.",

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N2 - A subcutaneous injection of 0.5 mg/kg 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), a drug with high affinity for 5-hydroxytryptamine (5-HT1A) binding sites, substantially increased eating in non-deprived rats. Intraventricular injections of 5,7-dihydroxytryptamine (5,7-DHT), a neurotoxin for 5-HT neurons, also significantly increased eating in rats and antagonized the effect of 8-OH-DPAT. Microinjections of 8-OH-DPAT (0.5 and 1 μg) in the nuclei dorsalis and medianus raphe also significantly increased eating in rats. 8-OH-DPAT appears to stimulate eating by acting on 5-HT-containing neurons. These results are compatible wwith the hypothesis that a decrease in central 5-HT function disinhibits feeding.

AB - A subcutaneous injection of 0.5 mg/kg 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), a drug with high affinity for 5-hydroxytryptamine (5-HT1A) binding sites, substantially increased eating in non-deprived rats. Intraventricular injections of 5,7-dihydroxytryptamine (5,7-DHT), a neurotoxin for 5-HT neurons, also significantly increased eating in rats and antagonized the effect of 8-OH-DPAT. Microinjections of 8-OH-DPAT (0.5 and 1 μg) in the nuclei dorsalis and medianus raphe also significantly increased eating in rats. 8-OH-DPAT appears to stimulate eating by acting on 5-HT-containing neurons. These results are compatible wwith the hypothesis that a decrease in central 5-HT function disinhibits feeding.

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