Journal: Biomedicines

Article Title: The Effects of Antipsychotics in Experimental Models of Krabbe Disease

doi: 10.3390/biomedicines11051313

Figure Lengend Snippet: Antipsychotics prevent psychosine toxicity of human astrocytes. ( a ) The experimental schematic diagram for treatment timelines prior to analysis. ( b ) Light microscopy images of astrocytes. ( c ) MTT assays of psychosine-induced cell toxicity in human astrocytes. Positive control of 20% DMSO. Kruskal-Wallis, Dunn’s multiple comparison tests ( n = 5–10). ( d ) LDH assays of psychosine-induced cell toxicity in human astrocytes. One-way ANOVA, Tukey’s multiple comparison tests ( n = 5). MTT assays showed that typical ( e ) 1 µM or ( f ) 10 µM and atypical ( h ) 1 µM or ( i ) 10 µM antipsychotics did not alter cell viability compared to control, while DMSO (20%) and psychosine (10 µM) significantly reduced cell viability compared to control ( p < 0.0001 #### ). All antipsychotics (1 µM or 10 µM) (except aripiprazole (Ari) at 10 µM) significantly prevented psychosine (10 µM) induced reductions in cell viability ( p < 0.05 *, p < 0.01 **, p < 0.001 *** and p < 0.0001 ****). Kruskal-Wallis, Dunn’s multiple comparison tests ( n = 5–10). LDH assays showed that ( g ) typical and ( j ) atypical antipsychotics at 1 µM were not toxic to cells compared to control, whereas DMSO (20%) and psychosine (10 µM) significantly increased cell toxicity compared to control. All antipsychotics (1 µM) prevented psychosine (10 µM) toxicity. One-way ANOVA, Tukey’s multiple comparison test ( n = 5). ( k ) Typical antipsychotics and ( l ) atypical antipsychotics (1 µM) had no effect alone on astrocyte morphology compared to control, while DMSO (20%) and psychosine (10 µM) reduced the number of astrocyte extensions. ( k ) Typical antipsychotics and ( l ) atypical antipsychotics (1 µM) attenuated morphological changes induced by 10 µM psychosine. Representative confocal cell fluorescent images labelled for GFAP (green), Vimentin (red) and Hoescht (blue). The number of astrocyte projections of 20–30 cells per treatment group was analysed. Images were analysed using ImageJ software. One-way ANOVA, Tukey’s multiple comparison tests ( n = 6). Typical antipsychotics included: Haloperidol (Hal), chlorpromazine (Chl) and sulpiride (Sul). Atypical antipsychotics included: clozapine (Clo), olanzapine (Ola), amisulpride (Ami), quetiapine (Que), risperidone (Ris) and aripiprazole (Ari).

Article Snippet: Compounds were reconstituted in dimethyl sulfoxide (DMSO, Sigma, Darmstadt, Germany; D8418) at stock concentrations of 5 mM and 20 mM depending on solubility, and were as follows: Clozapine (Cayman, Ann Arbor, MI, USA; 12059), Olanzapine (Cayman, Ann Arbor, MI, USA; 11937), Amisulpride (Cayman, Ann Arbor, MI, USA; 14619), Quetiapine (Acros organics, Geel, Belgium; 462400050), Risperidone (TCI, Tokyo, Japan; R0087), Aripiprazole (TargetMol, Wellesley Hills, MA, USA; T1566), Haloperidol (TCI, Tokyo, Japan; H0912), Chlorpromazine (TargetMol, Wellesley Hills, MA, USA; T1384), Sulpiride (TargetMol, Wellesley Hills, MA, USA; T1201) Eticlopride (Merck, Darmstadt, Germany; E101) and Volinanserin (Merck, Darmstadt, Germany; M3324).

Techniques: Light Microscopy, Positive Control, Comparison, Control, Software

Journal: Biomedicines

Article Title: The Effects of Antipsychotics in Experimental Models of Krabbe Disease

doi: 10.3390/biomedicines11051313

Figure Lengend Snippet: Selective D 2 and 5HT 2A antagonists prevent psychosine-induced toxicity. ( a ) Pharmacology Heat Map. Receptor binding profiles of antipsychotics are shown. Inhibitory constant (Ki): 100 nM < Ki < 10,000 nM (weak, light grey), 10 nM < Ki < 100 (moderate, mid grey), 1 > Ki < 10 (strong, dark grey). All drugs are antagonists or inverse agonists at D2 and 5HT2A receptors apart from aripiprazole which is a partial agonist at these receptors. Haloperidol (Hal), chlorpromazine (Chl), sulpiride (Sul), clozapine (Clo), olanzapine (Ola), amisulpride (Ami), quetiapine (Que), risperidone (Ris) and aripiprazole (Ari) ( b ) MTT assays showed that 1 µM Eticlopride (ETI) (selective D 2 antagonist) and 1 µM Volinanserin (VOL) (selective 5HT 2A antagonist) did not alter cell viability compared to control, while DMSO (20%) and psychosine (10 µM) significantly reduced cell viability compared to control. Both 1 µM Eticlopride (ETI) and 1 µM Volinanserin (VOL) prevented significant reductions in cell viability induced by 10 µM psychosine Kruskal-Wallis, Dunn’s multiple comparison tests ( n = 5). ( c ) LDH assays showed that 1 µM Eticlopride (ETI) and 1 µM Volinanserin (VOL) did not induce cell toxicity compared to the control. In contrast, DMSO (20%) and psychosine (10 µM) significantly increased cell toxicity compared to the control (####). Both drugs prevented significant cell toxicity induced by 10 µM psychosine. One-way ANOVA, Tukey’s multiple comparison tests ( n = 5). Representative confocal cell fluorescent images labelled for ( d ) GFAP (green) and ( e ) Vimentin (red), with Hoescht (blue) staining. Eticlopride (ETI) and Volinanserin (VOL) at 1 µM had no effect alone on astrocyte morphology compared to control, while DMSO (20%) and psychosine (10 µM) reduced the number of astrocyte extensions. Both selective antagonists attenuated morphological changes induced by 10 µM psychosine. The number of ( f ) GFAP (green) and ( g ) Vimentin (red) positive astrocyte projections of 20–30 cells per treatment group were analysed. Images were analysed using ImageJ software. One-way ANOVA, Tukey’s multiple comparison tests ( n = 6). p < 0.01 **, p < 0.001 *** and p < 0.0001****.

Article Snippet: Compounds were reconstituted in dimethyl sulfoxide (DMSO, Sigma, Darmstadt, Germany; D8418) at stock concentrations of 5 mM and 20 mM depending on solubility, and were as follows: Clozapine (Cayman, Ann Arbor, MI, USA; 12059), Olanzapine (Cayman, Ann Arbor, MI, USA; 11937), Amisulpride (Cayman, Ann Arbor, MI, USA; 14619), Quetiapine (Acros organics, Geel, Belgium; 462400050), Risperidone (TCI, Tokyo, Japan; R0087), Aripiprazole (TargetMol, Wellesley Hills, MA, USA; T1566), Haloperidol (TCI, Tokyo, Japan; H0912), Chlorpromazine (TargetMol, Wellesley Hills, MA, USA; T1384), Sulpiride (TargetMol, Wellesley Hills, MA, USA; T1201) Eticlopride (Merck, Darmstadt, Germany; E101) and Volinanserin (Merck, Darmstadt, Germany; M3324).

Techniques: Binding Assay, Control, Comparison, Staining, Software

Journal: Cells

Article Title: Quetiapine Ameliorates MIA-Induced Impairment of Sensorimotor Gating: Focus on Neuron-Microglia Communication and the Inflammatory Response in the Frontal Cortex of Adult Offspring of Wistar Rats

doi: 10.3390/cells11182788

Figure Lengend Snippet: The groups of the offspring generated and subsequently subjected to the administration of the antipsychotic drugs. The number of animals in each group is reported.

Article Snippet: Aripiprazole (Carbosynth, Berkshire, UK) was dissolved in 5% dimethyl sulfoxide (BioShop, Burlington, ON, Canada) in 1 mL of saline to a concentration of 1 mg/kg [ , ].

Techniques: Generated, Control

Journal: Cells

Article Title: Quetiapine Ameliorates MIA-Induced Impairment of Sensorimotor Gating: Focus on Neuron-Microglia Communication and the Inflammatory Response in the Frontal Cortex of Adult Offspring of Wistar Rats

doi: 10.3390/cells11182788

Figure Lengend Snippet: The impact of 14-day intraperitoneal administration of chlorpromazine, quetiapine or aripiprazole on the prepulse inhibition (PPI) of the acoustic startle response in the control and prenatally LPS-exposed offspring in adulthood. The numbers of animals in the cohorts were as follows: n = 4–13 (chlorpromazine), n = 9 (quetiapine) and n = 7 (aripiprazole) in each group. The results are presented as the means of the percentage of PPI (%PPI) calculated from the maximum startle response (V max ) ( A ) and average startle amplitude (AVG) ( B ) induced by each prepulse intensity ± SEM. # p < 0.05 vs. LPS + vehicle group.

Article Snippet: Aripiprazole (Carbosynth, Berkshire, UK) was dissolved in 5% dimethyl sulfoxide (BioShop, Burlington, ON, Canada) in 1 mL of saline to a concentration of 1 mg/kg [ , ].

Techniques: Inhibition, Control

Journal: Cells

Article Title: Quetiapine Ameliorates MIA-Induced Impairment of Sensorimotor Gating: Focus on Neuron-Microglia Communication and the Inflammatory Response in the Frontal Cortex of Adult Offspring of Wistar Rats

doi: 10.3390/cells11182788

Figure Lengend Snippet: The impact of prenatal exposure to LPS and subsequent chronic treatment with chlorpromazine ( A ), quetiapine ( B ) or aripiprazole ( C ) on Cx3cl1 , Cx3cr1 , Cd200 or Cd200r gene expression in the frontal cortices of the offspring. The mRNA levels were measured using qRT-PCR with n = 4–6 (chlorpromazine), n = 5–9 (quetiapine) and n = 5–6 (aripiprazole) in each group. The results are presented as the average fold change ± SEM. * p < 0.05 vs. control + vehicle group.

Article Snippet: Aripiprazole (Carbosynth, Berkshire, UK) was dissolved in 5% dimethyl sulfoxide (BioShop, Burlington, ON, Canada) in 1 mL of saline to a concentration of 1 mg/kg [ , ].

Techniques: Gene Expression, Control

Journal: Cells

Article Title: Quetiapine Ameliorates MIA-Induced Impairment of Sensorimotor Gating: Focus on Neuron-Microglia Communication and the Inflammatory Response in the Frontal Cortex of Adult Offspring of Wistar Rats

doi: 10.3390/cells11182788

Figure Lengend Snippet: The impact of prenatal exposure to LPS and subsequent chronic treatment with chlorpromazine ( A ), quetiapine ( B ) or aripiprazole ( C ) on Cd40 , Cd68 , Arg1 and Igf-1 gene expression in the frontal cortices of the offspring. The mRNA levels were measured using qRT-PCR with n = 4–6 (chlorpromazine), n = 6–9 (quetiapine) and n = 5–6 (aripiprazole) in each group. The results are presented as the average fold change ± SEM. * p < 0.05 vs. control + vehicle group, # p < 0.05 vs. LPS + vehicle group.

Article Snippet: Aripiprazole (Carbosynth, Berkshire, UK) was dissolved in 5% dimethyl sulfoxide (BioShop, Burlington, ON, Canada) in 1 mL of saline to a concentration of 1 mg/kg [ , ].

Techniques: Gene Expression, Control

Journal: Cells

Article Title: Quetiapine Ameliorates MIA-Induced Impairment of Sensorimotor Gating: Focus on Neuron-Microglia Communication and the Inflammatory Response in the Frontal Cortex of Adult Offspring of Wistar Rats

doi: 10.3390/cells11182788

Figure Lengend Snippet: The impact of prenatal exposure to LPS and subsequent chronic treatment with chlorpromazine ( n = 4–6 in each group), quetiapine ( n = 6 in each group) or aripiprazole ( n = 6–7 in each group) on the levels of the proinflammatory proteins (IL-1β, IL-6 and TNF-α) in the frontal cortices of the offspring. The results are presented as the mean ± SEM. * p < 0.05 vs. control + vehicle.

Article Snippet: Aripiprazole (Carbosynth, Berkshire, UK) was dissolved in 5% dimethyl sulfoxide (BioShop, Burlington, ON, Canada) in 1 mL of saline to a concentration of 1 mg/kg [ , ].

Techniques: Control

Journal: Cells

Article Title: Quetiapine Ameliorates MIA-Induced Impairment of Sensorimotor Gating: Focus on Neuron-Microglia Communication and the Inflammatory Response in the Frontal Cortex of Adult Offspring of Wistar Rats

doi: 10.3390/cells11182788

Figure Lengend Snippet: The impact of prenatal exposure to LPS and subsequent chronic treatment with chlorpromazine ( n = 4–6 in each group), quetiapine ( n = 6 in each group) or aripiprazole ( n = 6–7 in each group) on the levels of the anti-inflammatory proteins (IL-4 and IL-10) in the frontal cortices of the offspring. The results are presented as the mean ± SEM. * p < 0.05 vs. control + vehicle.

Article Snippet: Aripiprazole (Carbosynth, Berkshire, UK) was dissolved in 5% dimethyl sulfoxide (BioShop, Burlington, ON, Canada) in 1 mL of saline to a concentration of 1 mg/kg [ , ].

Techniques: Control

Journal: ACS Omega

Article Title: Involvement of Integrated Stress Response in Drug-Induced Secondary Dystonia

doi: 10.1021/acsomega.5c06867

Figure Lengend Snippet: (A) Aripiprazole induces ISR in N2a cells. N2a cells were treated with the indicated concentrations of aripiprazole (ARI) for 24 h or 5 μg/mL tunicamycin (TM). The cell extracts were analyzed by Western blot analysis with anti-ATF4, anti-CHOP, and anti-β actin antibodies. The analysis was repeated three times, and a representative blot is shown. (B) Aripiprazole induces ISR in N2a cells via activation of PERK and PKR. N2a cells were treated with the indicated concentrations of aripiprazole for 24 h. The cell extracts were analyzed by Western blot analysis with anti-PERK, anti-p-PKR. Anti-PKR, anti-p-eIF2α, and anti-eIF2α antibodies. One the three representative blots is shown.

Article Snippet: All antipsychotics were purchased from MedChemExpress (MCE): aripiprazole (HY-14546), haloperidol (HY-14538), paroxetine (HY-B0492), fluvoxamine (HY-B0103), trazodone (HY-B0478), nefazodone (HY-B1396), sertraline (HY-B01176A), and olanzapine (HY-14541).

Techniques: Western Blot, Activation Assay

Journal: ACS Omega

Article Title: Involvement of Integrated Stress Response in Drug-Induced Secondary Dystonia

doi: 10.1021/acsomega.5c06867

Figure Lengend Snippet: (A) Effect of inhibiting GCN2, PERK, and PKR on ATF4 induction in response to aripiprazole. N2a cells were pretreated with the indicated ISR kinase inhibitors for 2 h and then treated with aripiprazole for 24 h. The cell extracts were analyzed by Western blot analysis with anti-ATF4, anti-CHOP, and anti-β actin antibodies. The analysis was repeated three times, and a representative blot is shown. (B) Co-IP analysis to test for PACT–PKR interaction after treatment with aripiprazole. N2a cells were treated with 5 μg/mL tunicamycin (Tun) or 200 ng/mL aripiprazole (ARI). The cell extracts were prepared at 2 h after tunicamycin treatment and 24 h after aripiprazole treatment, and endogenous PKR protein was immunoprecipitated using anti-PACT mAb and protein A-sepharose. The immunoprecipitates were analyzed by Western blot analysis with anti-PKR monoclonal antibody (Co-IP panel). The blot was stripped and reprobed with anti-PACT mAb to ascertain an equal amount of PACT was immunoprecipitated in each lane (IP panel). Input blots: Western blot analysis of total proteins in the extract with anti-PACT and anti-PKR mAbs showing equal amount of PACT and PKR in all samples.

Article Snippet: All antipsychotics were purchased from MedChemExpress (MCE): aripiprazole (HY-14546), haloperidol (HY-14538), paroxetine (HY-B0492), fluvoxamine (HY-B0103), trazodone (HY-B0478), nefazodone (HY-B1396), sertraline (HY-B01176A), and olanzapine (HY-14541).

Techniques: Western Blot, Co-Immunoprecipitation Assay, Immunoprecipitation

Journal: ACS Omega

Article Title: Involvement of Integrated Stress Response in Drug-Induced Secondary Dystonia

doi: 10.1021/acsomega.5c06867

Figure Lengend Snippet: (A) Co-IP analysis to test the effect of luteolin on PACT–PKR interaction. N2a cells were either treated with 200 ng/mL aripiprazole 24 h (ARI) or pretreated with 50 μM luteolin followed by a 24 h treatment with 200 ng/mL aripiprazole (LUT+ARI). The endogenous PKR protein was immunoprecipitated from the cell extracts using anti-PKR mAb and protein A-sepharose. The immunoprecipitates were analyzed by Western blot analysis with anti-PACT monoclonal antibody (Co-IP panel). The blot was stripped and reprobed with anti-PKR mAb to ascertain an equal amount of PKR was immunoprecipitated in each lane (IP panel). Input blot: Western blot analysis of total proteins in the extract with anti-PACT and anti-PKR mAbs showing equal amount of PACT and PKR in all samples. (B) Effect of luteolin on ISR induction. N2a cells were either treated with 200 ng/mL aripiprazole 24 h (ARI) or pretreated for 24 h with 50 μM luteolin followed by a 24 h treatment with 200 ng/mL aripiprazole (LUT+ARI). The cell extracts were analyzed by Western blot analysis with anti-ATF4, anti-CHOP, anti-p-PKR. Anti-PKR, anti-p-eIF2α, anti-eIF2α, and anti-β-actin antibodies. One of the three representative blots is shown.

Article Snippet: All antipsychotics were purchased from MedChemExpress (MCE): aripiprazole (HY-14546), haloperidol (HY-14538), paroxetine (HY-B0492), fluvoxamine (HY-B0103), trazodone (HY-B0478), nefazodone (HY-B1396), sertraline (HY-B01176A), and olanzapine (HY-14541).

Techniques: Co-Immunoprecipitation Assay, Immunoprecipitation, Western Blot

Journal: FEBS Open Bio

Article Title: Dopamine receptor D 2 activation suppresses the radiosensitizing effect of aripiprazole via activation of AMPK

doi: 10.1002/2211-5463.12699

Figure Lengend Snippet: Treatment with a D2R‐selective antagonist augments aripiprazole‐induced apoptosis in human breast cancer cells. (A) Cells were treated with indicated concentrations of aripiprazole for 48 h. Cell viability was then determined using an EZ‐Cytox Cell Viability Assay Kit. Data represent means ± SD of three independent experiments (Student’s t ‐test; * P < 0.05). (B) Cleavage of PARP was examined by western blotting at the indicated time points after treatment with 20 µm aripiprazole. (C) Cells were treated with 20 µm aripiprazole for 40 h. Internucleosomal DNA fragmentation was then measured using the Cell Death Detection ELISA PLUS Kit (Roche). Data represent means ± SD of three independent experiments (Student’s t ‐test; * P < 0.05). (D) MCF‐7 cells were treated with 20 µm aripiprazole or indicated concentrations of quinpirole for 24 h. Cleavage of PARP was then examined by western blotting. (E) MCF‐7 cells were pretreated for 1 h with or without 2 µm thioridazine and subsequently treated with or without 20 µm aripiprazole for 16 h. Cleavage of PARP was then determined by western blotting. (F) MCF‐7 cells were pretreated with or without 10 µm haloperidol for 1 h and subsequently treated with or without 20 µm aripiprazole. Cleavage of PARP was then determined by western blotting.

Article Snippet: Aripiprazole, quinpirole, and haloperidol were purchased from Tocris (Ellisville, MO, USA).

Techniques: Viability Assay, Western Blot, Enzyme-linked Immunosorbent Assay

Journal: FEBS Open Bio

Article Title: Dopamine receptor D 2 activation suppresses the radiosensitizing effect of aripiprazole via activation of AMPK

doi: 10.1002/2211-5463.12699

Figure Lengend Snippet: Treatment with A769662, a direct AMPK activator, blunts the enhancing effects of D2R‐selective antagonists on aripiprazole‐induced apoptosis. (A) Phosphorylation of AMPK and ACC was examined by western blotting at the indicated time points after treatment with 20 µm aripiprazole or 20 µm quinpirole in MCF‐7 cells. (B) Twenty‐four hours after transfection with luciferase siRNA (control) or AMPKα siRNA (siAMPK), MCF‐7 cells were treated with or without 20 µm aripiprazole for 16 h. Cleavage of PARP and phosphorylation of AMPK were then determined by western blotting. (C) MCF‐7 cells were pretreated for 1 h with or without 100 µm A769662 and subsequently treated with 20 µm aripiprazole for 16 h. Cleavage of PARP and phosphorylation of AMPK were then determined by western blotting. (D) MCF‐7 cells were pretreated for 1 h with or without 100 µm A769662 and subsequently treated with or without 2 µm thioridazine for another 1 h. Cleavage of PARP and phosphorylation of AMPK were then determined by western blotting at 16 h after 20 µm aripiprazole treatment in the MCF‐7 cells. (E) MCF‐7 cells were pretreated for 1 h with or without 100 µm A769662 and subsequently treated with or without 10 µm haloperidol for another 1 h. Cleavage of PARP and phosphorylation of AMPK were then determined by western blotting at 16 h after 20 µm aripiprazole treatment in the MCF‐7 cells.

Article Snippet: Aripiprazole, quinpirole, and haloperidol were purchased from Tocris (Ellisville, MO, USA).

Techniques: Phospho-proteomics, Western Blot, Transfection, Luciferase, Control

Journal: FEBS Open Bio

Article Title: Dopamine receptor D 2 activation suppresses the radiosensitizing effect of aripiprazole via activation of AMPK

doi: 10.1002/2211-5463.12699

Figure Lengend Snippet: D2R‐selective antagonists augment the radiosensitizing effects of aripiprazole in human breast cancer cells. (A) MCF‐7 cells were pretreated for 1 h with or without the indicated concentration of aripiprazole. Cleavage of PARP was then determined by western blotting at 24 h after treatment of the MCF‐7 cells with 5 Gy of IR. (B) MCF‐7 cells were pretreated for 1 h with or without 20 µm aripiprazole. Internucleosomal DNA fragmentation was then measured using the Cell Death Detection ELISA PLUS Kit (Roche) at 40 h after treatment of the MCF‐7 cells with 5 Gy of IR. Data represent means ± SD of three independent experiments (Student’s t ‐test; * P < 0.05). (C) MCF‐7 cells were pretreated for 1 h with or without 2 µm thioridazine and subsequently treated with or without 20 µm aripiprazole for another 1 h. Cleavage of PARP and phosphorylation of AMPK were then determined by western blotting at 16 h after treatment of the MCF‐7 cells with 5 Gy of IR. (D) Cells were pretreated for 1 h with or without 2 µm thioridazine and subsequently treated with or without 20 µm aripiprazole for another 1 h. Internucleosomal DNA fragmentation was then measured by using Cell Death Detection ELISA PLUS Kit (Roche) at 40 h after treatment of the cells with 5 Gy of IR. Data represent means ± SD of three independent experiments (Student’s t ‐test; * P < 0.05). (E) MCF‐7 cells were pretreated for 1 h with or without 10 µm haloperidol and subsequently treated with or without 20 µm aripiprazole for another 1 h. Cleavage of PARP and phosphorylation of AMPK were then determined by western blotting at 16 h after treatment of the MCF‐7 cells with 5 Gy of IR. (F) Cells were pretreated for 1 h with or without 10 µm haloperidol and subsequently treated with or without 20 µm aripiprazole for another 1 h. Internucleosomal DNA fragmentation was then measured using Cell Death Detection ELISA PLUS Kit (Roche) at 40 h after treatment of the MCF‐7 cells with 5 Gy of IR. Data represent means ± SD of three independent experiments (Student’s t ‐test; * P < 0.05). (G) MCF‐7 cells were pretreated for 1 h with or without 100 µm A769662 and subsequently treated with 20 µm aripiprazole for another 1 h. Cleavage of PARP and phosphorylation of AMPK were then determined by western blotting at 16 h after treatment of the MCF‐7 cells with 5 Gy of IR. (H) Twenty‐four hours after transfection with luciferase siRNA (control) or AMPKα siRNA (siAMPK), MCF‐7 cells were pretreated for 1 h with or without 20 µm aripiprazole. Cleavage of PARP and phosphorylation of AMPK were then determined by western blotting at 16 h after treatment of the MCF‐7 cells with 5 Gy of IR. (I) Schema showing the nullifying contribution of D2R/AMPK pathway to the radiosensitizing effects of aripiprazole in breast cancer cells.

Article Snippet: Aripiprazole, quinpirole, and haloperidol were purchased from Tocris (Ellisville, MO, USA).

Techniques: Concentration Assay, Western Blot, Enzyme-linked Immunosorbent Assay, Phospho-proteomics, Transfection, Luciferase, Control