Disease relevance of quipazine

• At 0.01 mg/kg, LY 53857 attenuated quipazine-induced hypertension, whereas 0.003 mg/kg was ineffective [1].
• In both, the quipazine-evoked tachycardia was unaffected [2].
• In mice, quipazine has shown several behavioral effects: It antagonizes hypothermia induced by a high dose of apomorphine without altering climbing or stereotyped behavior; it antagonizes oxotremorine-induced hypothermia without altering tremors or peripheral signs; and it increases the toxicity of yohimbine [3].
• 5-HT2+IC antagonists, mesulergine and ketanserin, and 5-HT3 antagonists, quipazine and 3-tropanyl-indole-3-carboxylate, did not significantly attenuate 5-HT hyperalgesia [4].
• Superfusion of the ganglion with quipazine at a concentration of 1 microM produced complete blockade of responses to 5-HT in 3 of 6 ganglia and reduced responses by over 90% in 2 others; responses to DMPP were potentiated in amplitude and duration [5].

Psychiatry related information on quipazine

• Repeated electroconvulsive shock enhanced the locomotor activity produced by either quipazine (25 mg/kg i.p.) or apomorphine (0.2 mg/kg s.c.) compared to sham-shocked controls [6].
• Treatment with methysergide maleate (5 mg/kg, IP) 15 min before the administration of quipazine blocked quipazine-induced suppression of flow-wave sleep (SWS), but failed to prevent the decrease in rapid-eye-movement sleep (REMS) produced by quipazine [7].
• Administration of quipazine resulted in a decrease of median raphé self-stimulation at 5.0 and 7.1 mg/kg [8].
• The results show that quipazine reduces REM sleep rebound and that it has a biphasic effect on slow-wave sleep: initial 6 hr suppression is followed by a delayed increase in the second 24 hr recording period [9].
• Thus, cyclazocine may disrupt operant responding by impairing cognition, while quipazine may act through food satiation mechanisms [10].

High impact information on quipazine

• We have found that, in contrast to F344/N rats, LEW/N rats had markedly impaired plasma corticotropin and corticosterone responses to SCW, recombinant human interleukin 1 alpha, the serotonin agonist quipazine, and synthetic rat/human corticotropin-releasing hormone [11].
• This effect was selective for cell type because serotonin or quipazine (100 microM) did not increase prostacyclin synthesis by bovine aortic endothelial cells [12].
• Qualitative and theoretical quantitative structure-affinity relationship studies were carried out, and the interaction model for the 5-HT3 ligands related to quipazine with their receptor, proposed in part 1 of the present work, was updated to incorporate the latest data [13].
• Treatment of cells with random, sense, or mismatch oligodeoxynucleotide did not alter the stimulation of PI hydrolysis by quipazine or 5-HT2A receptor number [14].
• The rate of onset of the inhibitory effect of bath-applied 5-HT was slowed in the presence of (+)-tubocurarine but not in the presence of quipazine [15].

Chemical compound and disease context of quipazine

• In the present study, we tested whether administration of serotonin or its agonist quipazine could restore motor activity in a model of paraplegia [16].
• Fluoxetine, an inhibitor of 5-HT reuptake, had no effect, whereas quipazine (6 mg kg-1, i.p.), a 5-HT agonist, totally prevented the hypothermia [17].
• Last, 1-(4-iodo-2,5-dimethoxy-phenyl)-2-aminopropane- and quipazine-elicited head shakes, a 5-HT2A receptor-mediated response, were increased in the SHR strain compared with the LEW strain; on the other hand, 1-(3-chlorophenyl)piperazine triggered similar 5-HT2B/2C receptor-mediated decreases in motor activity in the two strains [18].
• 4. The data indicate that cardiovascular responses caused by i.c.v. quipazine and DOI are primarily due to activation of central 5-HT2A receptors, which causes the release of vasopressin and a tachycardia [2].
• Serotonin, its precursor 5-hydroxytryptophan or the receptor agonist, quipazine reversed the reserpine-induced hyperalgesia [19].

Biological context of quipazine

• Compound 5j acted as a 5-HT3 agonist in this assay with an EC50 value close to that reported for quipazine, while 5b was a partial agonist with an EC50 value of about 0.25 nM, and compound 5c possessed antagonist properties with an IC50 value (approximately 8 nM) in the same range as those of previously characterized 5-HT3 receptor antagonists [20].
• Discriminative stimulus properties of quipazine: mediation by serotonin2 binding sites [21].
• Quipazine reduces food intake in the rat by activation of 5-HT2-receptors [22].
• The present study examined the effects of quipazine on mean arterial pressure (MAP), heart rate (HR) and PRA in conscious, chronically catheterized male rats [1].
• Down-regulation of the protein kinase C isozymes alpha and epsilon by overnight exposure to phorbol-12,13-dibutyrate attenuated the intermediate phase (i.e., after 2-6 hr of agonist exposure) of DOI- and quipazine-induced desensitization [23].

Anatomical context of quipazine

• Effect of robotic-assisted treadmill training and chronic quipazine treatment on hindlimb stepping in spinally transected rats [24].
• Involvement of the locus coeruleus in the potentiation of the quipazine-induced head-twitch response by diazepam and beta-adrenoceptor agonists [25].
• Lesions of intergeniculate leaflet and serotonin afferents to the suprachiasmatic nucleus did not reduce the photic-like effects of quipazine, whereas bilateral enucleation and the subsequent degeneration of the retinohypothalamic tract abolished both the phase-shifting and the FOS-inducing effects of quipazine [26].
• Quipazine or vehicle was administered to the lumbar spinal cord using an intrathecal cannula [24].
• However, agonists, quipazine and trifluoromethylphenylpiperazine, with greater reported affinities for 5HT binding sites on rat brain membranes than MK212 were without effect as were the antagonists metergoline, methysergide, cyproheptadine, mianserine and methiothepin [27].

Associations of quipazine with other chemical compounds

• The 5-HT1A agonists 8-hydroxy-2-(di-n-propylamino)tetralin, ipsapirone, and 5-methoxy-N,N-dimethyltryptamine, the 5-HT1B agonist m-trifluoromethylphenylpiperazine, and the 5-HT2 agonist quipazine affected startle reactivity rather than having specific effects on habituation [28].
• Arylpiperazines, such as 1-(3-trifluoromethylphenyl)piperazine (TFMPP) and its chloro analogue mCPP, are 5-HT1 agonists, whereas quipazine, i.e., 2-(1-piperazino)quinoline, appears to be a 5-HT2 agonist [29].
• (2) Section of the forebrain, caudal to the frontal cortex (rich in 5-HT2 receptors), did not modify the effects of coerulean activity of quipazine-ketanserin injected systemically: quipazine induced an inhibition which was reversed by ketanserin [30].
• Doses of d-amphetamine (3.2 mg/kg), fenfluramine (10 mg/kg) and quipazine (8 mg/kg) cause a significant reduction in food intake during a 30-min daily feeding session in food-deprived rats [31].
• Discriminative-stimulus effects of quipazine and l-5-hydroxytryptophan in relation to serotonin binding sites in the pigeon [32].

Gene context of quipazine

• The nonspecific 5-HT receptor agonist (and 5-HT2 receptor antagonist) quipazine also induced "wet dog shaking" at doses which suppressed aggression, social interest, and exploration but increased inactive behaviors (sitting and lying) [33].
• Intrathecal administration of 5-HT3 receptor agonist quipazine (200 mg) abolished nociceptive flexion reflex and alleviated spinal pain syndrome produced by impairment of GABAergic inhibition in the lumbar spinal segments [34].
• Previous data showed that an acute administration of a 5-HT2 agonist (quipazine) could promote motor function recovery in spinal rats [35].
• Both beta 1-and beta 2-adrenoceptor agonists potentiated the head-twitch induced by quipazine in sham-operated controls [25].
• Other serotonergic compounds failed to produce substantial BMY 14802-appropriate responding; such as 5-HT1 agonist I-5-HTP; 5-HT1A/1B agonist RU24969; 5-HT1B/1C agonist m-CPP; 5-HT1C/2 agonist quipazine; 5-HT1C/2 antagonists, metergoline and the atypical antipsychotic clozapine; and 5-HT3 antagonist ondansetron [36].

Analytical, diagnostic and therapeutic context of quipazine

• After quipazine administration, a significant increase in intracellular immunofluorescence was measured [37].
• Purification was achieved by affinity chromatography using immobilized GR119566X and biospecific elution with quipazine [38].
• Following a selective denervation of 5-HT neurones with intraventricular injection of 5,7-di-hydroxy-tryptamine in desipramine-pretreated rats, the responsiveness of neurones in the ventral lateral geniculate nucleus to quipazine, applied microiontophoretically, was increased as was that to 5-HT and to LSD [39].
• However, continuous subdural perfusion of quipazine via an osmotic pump over 1 month proved to be more effective [35].
• In a likewise manner, intra-SCN microinjection of quipazine inhibited light-induced Fos-LI in the ventrolateral SCN, indicating that the suppressive action of quipazine is centered in the SCN [40].

References