Receptor binding properties of amperozide

Svartengren, Jan; Simonsson, Per

doi:10.1111/j.1600-0773.1990.tb01599.x

Cited by 66 publications

(34 citation statements)

References 23 publications

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“…Correspondence to: K. Uvn/is-Moberg the drug is a potent 5-hydroxytryptamine (5-HTz) receptor antagonist and shows a moderate affinity for eladrenoceptors (Svartengren and Simonsson 1990). Like the atypical neuroleptic drug clozapine, amperozide appears to selectively affect the mesolimbocortical DA system in the brain with only negligible effects on the nigrostriatal DA pathway (Gustafsson and Christensson 1990).…”

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confidence: 99%

Amperozide and clozapine but not haloperidol or raclopride increase the secretion of oxytocin in rats

1992

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The aim of the present study was to investigate whether amperozide, an antipsychotic drug which possesses anti-aggressive and anxiolytic-like properties, stimulates the secretion of oxytocin and if so, by which receptor mechanism. For this purpose, female or male Sprague Dawley rats were given amperozide (0.5, 2.5 and 5.0 mg/kg IP), ritanserin (5.0 mg/kg), raclopride (2.0 mg/kg) and prazosin (1.0 mg/kg) and were subsequently decapitated for collection of blood (30 and 120 min) after injection. Oxytocin levels were measured with radioimmunoassay. Amperozide 2.5 and 5 mg/kg increased plasma levels of oxytocin significantly (P < 0.05 and < 0.001). The effect appeared maximal about 30 min after injection of the drug and oxytocin levels were almost back to basal within 120 min. Similar effects were obtained in female and male rats as well as in animals that were freely fed or food deprived for 24 h. CSF levels of oxytocin were also increased. Ritanserin, a 5-HT2-receptor antagonist but not the D2 receptor antagonist raclopride or the alpha 1-adrenoceptor antagonist prazosin stimulated oxytocin release. In addition, clozapine, a neuroleptic with potent HT2-antagonistic properties, was a potent releaser of oxytocin, whereas haloperidol was without effect. A possible role for oxytocin in the behavioural effects of amperozide and clozapine remains to be explored.

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Amperozide and clozapine but not haloperidol or raclopride increase the secretion of oxytocin in rats

1992

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“…Recent biochemical and electrophysiological studies have classified amperozide as a selective 5-HT 2A (serotonin type 2A) receptor antagonist [1,2]. However, few studies have classified amperozide's activity through behavioral means.…”

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Amperozide Influences Feeding Independently of 5-HT<sub>2A</sub> Receptor Antagonism

Price¹,

Gorzalka²,

White³

et al. 1998

Neuropsychobiology

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Amperozide has been biochemically classified as a selective 5-HT_2A (serotonin type 2A) receptor antagonist. However, research on the behavioral effects of amperozide suggests the possibility of other mechanisms. The present study in the male rat is an investigation of the effect of amperozide on feeding, a behavior which can be inhibited by 5-HT_2A agonists such as 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI). Experiments revealed that amperozide acted to inhibit feeding behavior both when administered alone and when administered in combination with DOI. These results are inconsistent with 5-HT_2A receptor antagonism by amperozide. Further experiments suggested that amperozide may be acting via α₂-adrenergic or 5-HT_1A receptors to inhibit feeding. These studies imply that amperozide’s selective 5-HT_2A antagonistic activity is behaviorally specific.

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“…1992). Amperozide also has moderate affinity for a,-adrenergic receptors, a weak affinity for D2 dopamine receptors (Svartengren & Simonsson 1990; McMillen et nl. 1993) In a behavioural model used to study drug addiction, amperozide significantly reduced a cocaine-induced conditioned place preference (Jones & McMillen 1995).…”

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“…1992). Amperozide also has moderate affinity for a,-adrenergic receptors, a weak affinity for D2 dopamine receptors (Svartengren & Simonsson 1990;McMillen et nl. 1993) and is a weak inhibitor of dopamine and 5-hydroxytryptamine uptake (Eriksson 1990: Eriksson & Christensson 1990.…”

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The Cardiovascular Effects of Amperozide: Interactions with Cocaine

Jones

McMillen

1999

Pharmacology & Toxicology

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Absrrwcr: Amperozide is a 5-HTZA receptor antagonist that significantly reduces the acquisition and expression, by rats, of a cocaine conditioned place preference. In order to rule out the possibility that amperozide affects a cocaine conditioned place preference due to effects on blood pressure or heart rate, the cardiovascular effects of amperozide were investigated. Alternating cumulative doses of amperozide (0.5, 1.0, 1.5 and 2.5 nig kg-l) or saline and phenylephrine (8 pg kg-I) were administered through the femoral vein of awake freely-moving Sprague-Dawley rats and blood pressure and heart rate were recorded from the femoral artery. A single dose of cocaine (5.0 mg kggl) was administered after all the amperozide or saline doses were given. Amperozide (0.5, 1.0, I .5 and 2.5 mg kg-I) did not have any significant effect on blood pressure compared to the saline control treatment to the same animals. However, 0.5 mg kg-I amperozide significantly decreased heart rate at 5 and 10 min. after administration, but higher doses did not further depress heart rate. Amperozide did not affect the increased blood pressure and decreased heart rate caused by phenylephrine, an al-adrenoceptor agonist. In addition, amperozide did not affect the cardiovascuhr response to an intravenous dose of 5.0 nig kg-I cocaine. These results suggest that amperozide does not cause direct cardiovascular effects. The mechanism by which the lowest dose of amperozide caused a decrease in heart rate is unknown. Amperozide affects neither a-adrenoceptor mediated vasoconstriction nor the increased sympathetic activity caused by the peripheral and central effects of cocaine. The significance of these results, in terms of locomotor activity and the cocaine conditioned place preference paradigm, is discussed.Amperozide is a novel putative antipsychotic drug characterized by high affinity for 5-hydro~ytryptamine~~ ( 5 -HTzA) receptors (Axelsson ef u/. 1991; Bjork et ul. 1992). Amperozide also has moderate affinity for a,-adrenergic receptors, a weak affinity for D2 dopamine receptors (Svartengren & Simonsson 1990; McMillen et nl. 1993) In a behavioural model used to study drug addiction, amperozide significantly reduced a cocaine-induced conditioned place preference (Jones & McMillen 1995). This report demonstrated that animals spent significantly more time in the cocaine associated chamber after repeated cocaine administration compared to the time spent in the cocaine-associated chamber before cocaine administration. Administration of amperozide prior to each dose of cocaine during the conditioning phase completely blocked a conditioned place preference. The mechanism by which amperozide reduced the cocaine-conditioned place preference is unknown. It is hypothesized that amperozide acts within the mesocorticolinibic system to inhibit the rewarding effects related to cocaine-associated conditioning cues, without a blockade of dopamine receptors (Jones & McMillen 1995). In the conditioned place preference paradigm, drugs are injected on training days...

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Receptor binding properties of amperozide

Cited by 66 publications

References 23 publications

Amperozide and clozapine but not haloperidol or raclopride increase the secretion of oxytocin in rats

Amperozide and clozapine but not haloperidol or raclopride increase the secretion of oxytocin in rats

Amperozide Influences Feeding Independently of 5-HT<sub>2A</sub> Receptor Antagonism

The Cardiovascular Effects of Amperozide: Interactions with Cocaine

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