Abilify ja kuukautiset
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7 Recomprehension Release Aripiprazole, a Novel Antipsychotic, Is a High-Affinity Partial Agonist at Human Dopamine D2 Receptors Aripiprazole is the first next-generation atypical antipsychotic with a mechanism of action that differs from currently marketed typical and atypical antipsychotics. Aripiprazole displays properties of an agonist and antagonist in animal models of dopaminergic hypoactivity and hyperactivity, respectively. This study examined the interactions of aripiprazole with a single population of human D2 receptors to clarify further its pharmacologic properties.

In membranes prepared from Chinese hamster ovary cells that express recombinant D2L receptors, aripiprazole bound with high affinity to both the G protein-coupled and uncoupled states of receptors. Aripiprazole potently activated D2 receptor-mediated inhibition of cAMP accumulation. Partial receptor inactivation using the alkylating agent N -ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline (EEDQ) significantly reduced the maximum effect of aripiprazole on inhibition of cAMP accumulation.

This effect was seen with concentrations of EEDQ that did not alter the maximal inhibitory effect of dopamine. Consistent with the expected effects of a partial agonist, increasing concentrations of aripiprazole blocked the action of dopamine with maximal blockade equal to the agonist effect of aripiprazole alone. The efficacy of aripiprazole relative to that of dopamine varied from 25% in cells that lacked spare receptors for dopamine to 90% in cells with receptor reserve. These results, together with previous studies demonstrating partial agonist activity at serotonin 5-hydroxytryptamine (5- HT)1A receptors and antagonist activity at 5-HT2A receptors, support the identification of aripiprazole as a dopamine- serotonin system stabilizer.

The receptor activity profile may underlie the unique activity of aripiprazole in animals and its antipsychotic activity in Aripiprazole, 7- -3,4-dihydro-2(1 H )-quinolinone, is the first next-generation atypical antipsychotic that is active against positive and negative symptoms of schizophrenia (Petrie et al.

2001 ), has a low propensity for extrapyramidal side effects (Petrie et al.

2001 ), causes minimal weight gain or sedation (Petrie at al. 2002 ), and produces no elevation in serum prolactin levels (Petrie et al. 2001 ) or prolongation of QTc interval on ECG (Kane et al.

The mechanism of action of aripiprazole differs from that of currently marketed typical and atypical antipsychotics. Previous preclinical studies have provided evidence that aripiprazole is a dopamine-serotonin system stabilizer with potent partial agonist activity at dopamine D2 and 5-HT1A receptors and antagonist activity at 5-HT2A receptors (Inoue et 1996 ; Jordan et al.

Like many antipsychotics, aripiprazole binds with high affinity to members of the D2 family of dopamine receptors (Kikuchi 1995 ;Lawler et al.

Whereas currently marketed antipsychotics are believed to exert their effects through antagonism of D2 (and possibly 5 -HT2) receptors (see Miyamoto et al.

2000 for a recent review), aripiprazole may exert its effects through partial agonism at D2 receptors. In multiple studies in vivo, aripiprazole has been shown to have potent agonist activity at dopamine autoreceptors.

For example, aripiprazole decreases -butyrolactone- and reserpine-induced DOPA accumulation (Kikuchi et al. 1995 ), consistent with a decrease in presynaptic tyrosine hydroxylase activity.

The inhibitory effect of aripiprazole on -butyrolactone-induced DOPA accumulation is blocked by the D2 receptor antagonist haloperidol.

Administration of aripiprazole to laboratory rats results in decreased extracellular levels of dopamine in the striatum and frontal cortex suggestive of decreased release of dopamine (Semba et al. Finally, the ability of aripiprazole to decrease spontaneous firing of dopaminergic neurons in the ventral tegmentum by activation of D2 autoreceptors was shown by extracellular recording in vivo (Momiyama et al. Whereas results of the above studies are consistent with agonist activity of aripiprazole at D2 receptors, in other in vivo studies, aripiprazole displays properties of a D2 receptor antagonist.

For example, aripiprazole blocks apomorphine-induced stereotypy and locomotor activity and does not produce stereotypy or increased locomotion when administered alone (Kikuchi et al.

Consistent with blockade of dopamine receptors coupled to the inhibition of prolactin release, administration of aripiprazole to male rats results in a 2-fold increase in levels of serum prolactin (Inoue et al.

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