Disease relevance of Amperozide

• Niether amperozide nor naltrexone exerted any significant effects on food and water intakes or on body weight [1].
• In Exp. 2 to 8, 1,648 pigs growing from approximately 20 to 100 kg body weight were used to determine the effect of amperozide on weight gain [2].
• The time to arrhythmia was significantly prolonged after treatment with amperozide, melperone and bretylium compared with saline, but there were no differences between the treatments [3].
• On the other hand, amperozide did not produce catalepsy, nor did it reverse amphetamine-induced stereotypies [4].

Psychiatry related information on Amperozide

• Suppression of alcohol preference in high alcohol drinking rats: efficacy of amperozide versus naltrexone [1].
• Amperozide restored social interactions to near control levels and elevated social interactions in the animals treated with saline vehicle [5].
• The increase in extracellular 5-HT levels in the medial prefrontal cortex or nucleus accumbens following amperozide, clozapine, or risperidone administration may not be related to the effect on psychotic symptoms but could be related to effects on other types of psychopathology such as depression, negative symptoms, or cognition [6].
• These complex findings suggest that biochemical properties other than 5-HT2A receptor antagonism (e.g., 5-HT1A receptor agonism) may be involved in the effects of amperozide and FG 5974 on alcohol intake and other consummatory behaviors [7].
• Two of these drugs, FG5606 (amperozide) and FG 5893 are essentially "antialcoholic" or anticraving and are without any significant side effects on cerebral mechanisms responsible for hunger, caloric intake, motor activity, or other physiological process [8].

High impact information on Amperozide

• Interaction of the novel antipsychotic drug amperozide and its metabolite FG5620 with central nervous system receptors and monoamine uptake sites: relation to behavioral and clinical effects [9].
• In the present study amperozide displayed low affinity for several serotonin receptor subtypes as well as for the dopamine D4 receptor transfected in COS7 cells (Ki D4.2 = 769 nmol/L and Ki D4.4 = 384 nmol/L) [9].
• In addition, after amperozide the number of Fos-positive nuclei was higher in the nucleus accumbens than in the dorsolateral striatum, a characteristic that is common to all known atypical antipsychotic agents [10].
• The putative atypical antipsychotic drug amperozide preferentially increases c-fos expression in rat medial prefrontal cortex and lateral septum [10].
• With the exception of the nucleus accumbens-shell, where amperozide failed to produce statistically significant increases, the regional distribution of Fos immunoreactivity following amperozide was similar to that induced by atypical, but not by typical, antipsychotic drugs [10].

Chemical compound and disease context of Amperozide

• The lack of effect on the synthesis of dopamine and 5-HT and the absence of side effects on the intakes of food and water suggest that amperozide may be a specific agent for suppressing alcohol drinking [11].

Biological context of Amperozide

• Food intake was also suppressed by amperozide at higher doses, whereas it was increased by FG 5974 [7].
• Amperozide 4-[4,4-bis(4-fluorophenyl)butyl]-N-ethylpiperazine-1- carboxamide) is used in veterinary medicine because of its sedative effect on pigs [12].
• The suppressive effect of DOI was antagonized by treatment with amperozide, a selective 5-HT2 receptor antagonist, in doses which did not by themselves affect sexual activity [13].
• Immediately after the experimental treatment, the highest PBL reactivity was found for the amperozide-treated animals and for the non-transported animals, with no differences in reactivity between Hal genotypes [14].
• Because serotonergic neurons are implicated in both the central mechanisms underlying thermoregulation and the reinforcing effects of alcohol, this study was undertaken to determine whether the poikilothermic effects of alcohol on body temperature (Tb) would be altered by amperozide [15].

Anatomical context of Amperozide

• Amperozide (2-10 mg/kg, s.c.) significantly increased extracellular levels of DA in both the striatum and nucleus accumbens in a dose-dependent manner [16].
• Amperozide significantly increased the number of Fos-immunoreactive nuclei in the medial prefrontal cortex and the lateral septum but not in the nucleus accumbens (shell or core), the striatum, or the amygdala [10].
• The effects of acute, systemic administration of the putative atypical antipsychotic drug amperozide on c-fos expression in the rat forebrain were studied by means of Fos immunohistochemistry [10].
• The highest dose of amperozide inhibited the activity in substantia nigra pars compacta, showing a liability to induce extrapyramidal side-effects [17].
• Because amperozide acts centrally on the synaptic activity of dopaminergic and serotonergic neurons in limbic system structures, it is envisaged that the drug ameliorates the aberrant drinking of alcohol by virtue of a direct effect on either one or both of these classes of neurons.(ABSTRACT TRUNCATED AT 250 WORDS)[18]

Associations of Amperozide with other chemical compounds

• The effect of acute subcutaneous BIMG 80, clozapine, haloperidol, risperidone, amperozide, olanzapine, and Seroquel was then investigated on dopamine release in medial prefrontal cortex, nucleus accumbens, and striatum in freely moving rats using the microdialysis technique [19].
• 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 [20].
• In the present study, the effect of this compound on operant responding for ethanol (as well as water and a saccharin solution) was compared to compounds possessing the separate neuropharmacological effects of this drug (the 5-HT1A agonist, 8-OH-DPAT, and the 5-HT2A antagonist, amperozide) [21].
• Pretreatment with the other atypical APD (sulpiride, 30 mg/kg; amperozide, 1 mg/kg) had no effect on these three receptors, although at higher doses, sulpiride (60 mg/kg) and amperozide (5 mg/kg) slightly but significantly reversed D2 and 5-HT2 receptor inactivation, respectively [22].
• Three putative atypical antipsychotic agents melperone, amperozide and MDL 100907 did not bind with high affinities to either the 5-HT6 or 5-HT7 receptors (Kis > 50 nM) [23].

Gene context of Amperozide

• Both the 5-HT2 antagonist, FG5606 (amperozide), and the mixed 5-HT1 agonist/5-HT2 antagonist, FG5893, attenuate significantly the volitional intake of alcohol in the cyanamide treated rat [24].
• A possible role for oxytocin in the behavioural effects of amperozide and clozapine remains to be explored [20].
• The prolactin levels were not increased during amperozide treatment [25].
• Furthermore, amperozide did not attenuate d-fenfluramine-elicited prolactin release, which is known to be antagonized by ritanserin [26].
• The brain regional dopamine D2 receptor binding properties of amperozide were investigated by using in vitro and in vivo radioligand binding techniques [27].

Analytical, diagnostic and therapeutic context of Amperozide

• Single intraperitoneal injections of amperozide (0.2, 1, or 5 mg/kg) or FG5803 (1.2, 6, or 30 mg/kg) were without effect on oral behaviors [28].
• After oral administration, amperozide was also more effective than FG 5974 in reducing alcohol intake [7].
• A method developed for the detection of amperozide residues in porcine liver using liquid chromatography with thermospray mass spectrometry (LC-MS) is described and compared with LC with electrochemical detection (LC-ED) [12].
• Effects of amperozide in two animal models of anxiety [29].
• The effects of amperozide on sow performance when administered as a single intramuscular injection of 1 mg kg-1 at the time of either farrowing or weaning, or on both occasions were evaluated [30].

References