Disease relevance of Emergil

• Rats receiving cis-flupentixol demonstrated tolerance to its cataleptogenic effects, with a significant reduction in catalepsy observed by treatment day 7 [1].
• When applied alone, neither alpha-flupenthixol nor affected the activity of ganglion cells in adults, but in kittens both antagonists produced an excitatory effect in some cells [2].

Psychiatry related information on Emergil

• Reaction time was measured from the CS to the release of the lever for each trial. alpha-Flupenthixol (0.2 and 0.4 mg/kg) injected intraperitoneally impaired the reaction-time performance of the rats [3].
• Furthermore, the long-refractory period effects of MFB self-stimulation are reduced, but not completely blocked, by peripheral injections of alpha-flupenthixol, suggesting that dopamine axons make small contributions to MFB self-stimulation when small tips are used [4].
• Recent reports have suggested that neurotensin (NT) and some of its analogues resemble neuroleptics, for example alpha-flupenthixol (FLU), in their ability to suppress locomotor activity [5].
• Pretreatment with alpha-flupenthixol (0.8 mg/kg, i.p.) before morphine injections during the development of opiate dependence did not effect expression of withdrawal aversions or the expression of somatic withdrawal [6].
• Effects of bromocriptine and alpha-flupenthixol on sleep in REM sleep deprived rats [7].

High impact information on Emergil

• 6. Apomorphine (0.05-0.2 mg/kg, I.A.) inhibited the chemoreceptor discharge for up to 45 min, an effect which was antagonized by alpha-flupenthixol (0.2 mg/kg, I.A.), implying it resulted from DA receptor stimulation [8].
• Systemic injection of the mixed dopaminergic D1/D2 receptor antagonist, alpha-flupenthixol (0.03-0.18 mg/kg), reduced premature responses and perseverative panel pushing without affecting the perseverative nose-poke responses, suggesting that some of the deficits were independent of striatal dopaminergic transmission [9].
• Chlorpromazine produced the same increase in discharge rate, but was significantly less potent. alpha-Flupenthixol was equipotent with fluphenazine, but beta-flupenthixol, a behaviorally inactive stereoisomer, was without effect [10].
• There was a time lag of at least 2 weeks between the increase in prolactin secretion in patients on alpha-flupenthixol and the therapeutic effect attributable to medication [11].
• The effect of baclofen on alpha-flupenthixol-induced catalepsy in the rat [12].

Chemical compound and disease context of Emergil

• 1 alpha-Flupenthixol (alpha-FPT)-induced catalepsy in the rat was potentiated by diaminobutyric acid (DABA), an inhibitor of the neuronal high affinity uptake of gamma-aminobutyric acid (GABA) [13].

Biological context of Emergil

• The antagonists inhibited the dopamine-induced vasodilation in the following order of potency: (+)butaclamol greater than cis-flupentixol greater than haloperidol greater than bulbocapnine greater than sulpiride [14].
• In a temperature-gradient test paradigm (requiring less physical effort on the part of the subjects) alpha-flupenthixol did not alter the animals' preferred environmental temperature, nor did it disrupt behavioral thermoregulatory ability [15].
• Pharmacological characterization of the phenomenon indicated that it is mediated by stimulation of dopamine receptors, since pretreatment with haloperidol, cis-flupentixol but not with trans-flupentixol, completely prevent the reduction in blood pressure induced by dihydroergotoxine [16].

Anatomical context of Emergil

• When bilaterally injected into the nucleus accumbens before the test session, a dopamine receptor blocker, alpha-flupenthixol, blocked the expression of the amphetamine-conditioned place preference. alpha-Flupenthixol had no significant effect on spontaneous locomotor activity [17].
• cis-Flupentixol antagonism of the rat prefrontal cortex neuronal response to apomorphine and ventral tegmental area input [18].

Associations of Emergil with other chemical compounds

• Social isolation in the young rat: neurochemical effects of treatment with a long-acting neuroleptic, alpha-flupenthixol decanoate [proceedings] [19].
• Primary care treatment of depression in the elderly: a double-blind, multi-centre study of flupenthixol ('Fluanxol') and sustained-release amitriptyline [20].
• Retention was not affected by the injection of the D1-D2 receptor antagonist cis-flupentixol, but the preadministration of cis-flupentixol significantly blocked the facilitatory effect of nicotine and cytisine on memory [21].
• A triple dissociation in the effects of AP-5, LY293558 [(3SR, 4aRS, 6RS, 8aRS)-6-[2-(iH-tetrazol-5-yl)ethyl]-1,2,3,4,4a,5,6,7,8,8a-decahydroiso-quinoline-3-carboxylic acid], and alpha-flupenthixol infused into the nucleus accumbens core on the acquisition and performance of this conditioned response was observed [22].

Gene context of Emergil

• Differences in the interaction of trans- and cis-flupentixol with the phospholipids studied are suggested to be responsible for their different MDR-reversing ability [23].
• Cis (alpha)-flupenthixol and (+)-butaclamol are effective anti-psychotic agents but trans (beta)-flupenthixol and (-)-butaclamol are not. alpha-Flupenthixol was found to be 245 times more active in elevating rat plasma prolactin than the beta-isomer [24].
• Effects of alpha-flupenthixol and naloxone on CRF-induced locomotor activation [25].
• In the framework of the model, it is assumed that indirect dopaminergic (DA) agonists (e.g. amphetamine and nicotine) increase, and DA receptor antagonists (e.g. haloperidol and alpha-flupenthixol) decrease, the effect of Novelty on attention [26].
• Therefore a molecular modeling study of trans-(T) and cis-flupentixol (C) was performed in order to elucidate the observed discrepancy between equal binding potency to P-glycoprotein and different MDR reversing activity of the two stereoisomers [27].

Analytical, diagnostic and therapeutic context of Emergil

• Acc lesioned rats, the neuroleptic alpha-flupenthixol (0.1-1.0 mg/kg) led to fewer trials being completed and longer latencies than in the sham-operated control group [28].
• In experiment one it was found that amphetamine stimulated ipsiversive circling produced by unilateral SC lesions was additive with the ipsiversive circling produced by alpha-flupenthixol microinjections into the lateral SNC but was not additive with the contraversive circling produced by such injections into the medial SNC [29].

References