Bromocriptine is a potent dopamine D2/D3 receptor agonist, which binds D2 dopamine receptor with pK_i of 8.05±0.2. IC50 & Target: pKi: 8.05±0.2 (dopamine D2 receptor)^[1] In Vitro: Bromocriptine stimulates [³⁵S]-GTPγS binding at D2 dopamine receptor expressed in CHO cells with pEC₅₀ of 8.15±0.05^[1]. Bromocriptine also is a strong inhibitor of brain nitric oxide synthase. The ergot alkaloid Bromocriptine (BKT) is found to act as a strong inhibitor of purified neuronal nitric oxide synthase (NOS) (IC₅₀=10±2 μM) whereas it is poorly active towards inducible macrophage NOS (IC₅₀>100 μM) ^[2]. Bromocriptine is found to inhibit the activity of at least one human cytochrome P450 enzyme. Bromocriptine is a potent inhibitor of CYP3A4 with a calculated IC₅₀ value for the interaction of 1.69 μM^[3]. In Vivo: Bromocriptine (a dopamine agonist) treatment (2 mg/kg, i.p.) group shows significant anti-immobility action as compared to control. When Bromocriptine administered 30 min after the last dose of 7 days MPE treatment and subjected to FST, this dopaminergic agonist produces significant and dose dependent potentiation of anti-immobility action of MPE (200 mg/kg, p.o.) as compared to MPE treatment alone. Bromocriptine (a dopamine agonist) treatment (2 mg/kg, i.p.) group shows a significant reduction of immobility time as compared to control. Bromocriptine administration after 7 days pretreatment with MPE (100 and 200 mg/kg, p.o.) shows significant and dose dependent potentiation of anti-immobility action of MPE as compared to MPE treatment alone^[4]. Intraperitoneal administration of Bromocriptine induces a significant, dose dependent (0.1 mg and 1 mg/Kg) decrease in pain scores in CCI-IoN group when compared to sham and its effect lasted for 6 h. The highest dose induces the highest score decrease, (P<0.01). As a positive control SKF8129 (DR1 agonist) is used. Its intraperitoneal administration induces a non-significant increase in the SMA score when compared to sham (saline-injected). Intracisternal administration of Bromocriptine decreases significantly the SMA score when compared to sham (saline-injected). Bromocriptine effect lasted for 20 min. Intraperitoneal administration of Bromocriptine induces a significant dose dependent decrease in SMA score in CCI-IoN?+?6-OHDA lesioned group compared to that of sham. Its effect lasted for 6 h. SKF81297 administration increases the allodynic score. Intracisternal administration of Bromocriptine decreases significantly the SMA score compared to that of sham (saline-injected rats) and its effect lasted for 30 min^[5].