citalopram brands

Molecular formula: C20H21FN2O

The mechanism of action of citalopram is unclear but is presumed to be related to potentiation of serotonergic activity in the central nervous system (CNS) resulting from its inhibition of CNS neuronal reuptake of serotonin (5-HT), potentially through the inhibition of the serotonin transporter (solute carrier family 6 member 4, _SLC6A4_). Citalopram binds with significantly less affinity to histamine, acetylcholine, and norepinephrine receptors than tricyclic antidepressant drugs. Particularly, citalopram has no or very low affinity for 5-HT_1A, 5-HT_2A, dopamine D₁ and D₂, α₁-, α₂-, and β-adrenergic, histamine H₁, gamma aminobutyric acid (GABA), muscarinic cholinergic, and benzodiazepine receptors. /In/ whole-cell patch clamp recording of heterologous HERG-mediated currents in transfected mammalian cells ... citalopram blocks HERG with an IC(50) of 3.97 uM. This is slightly less potent than fluoxetine in /the same/ system (IC(50) of 1.50 uM). In isolated guinea pig ventricular cardiomyocytes, citalopram inhibited L-type calcium current (I(Ca,L)). The voltage dependence of I(Ca,L) inactivation in the presence of 100 uM citalopram was shifted significantly leftward. As a result, the I(Ca,L) 'window' in citalopram was found to be smaller & leftward-shifted compared to control. /These/ effects ... may help to explain citalopram's good cardiac safety profile, given its propensity to block HERG at excessive dosages. /Salt not specified/ The study was aimed to investigate the effects of the minimal effective doses of acute citalopram (5 mg/kg), (+/-)-8-hydroxydipropylaminotetralin HBr (8-OH-DPAT; 0.1 mg/kg), & their combined treatment on the rat open field & forced swimming behaviour & post-mortem monoamine content. The animals were prospectively divided into the vehicle- and para-chlorophenylalanine (p-CPA)-pretreated (350 mg/kg) groups. Acute citalopram (5 mg/kg), 8-OH-DPAT (0.1 mg/kg), or their combined treatment had no major effect on the rat open field & forced swimming behaviour. The post-mortem catecholamine content in four brain regions studied was unchanged in all treatment groups. The combined 8-OH-DPAT (0.1 mg/kg) & citalopram (5 mg/kg) treatment partially reversed the p-CPA-induced decr of serotonin (5-HT) and 5-hydroxy-indolacetic acid (5-HIAA) content. The present experiments demonstrate that the 5-HT1A receptors mediate some of the selective serotonin reuptake inhibitor-induced biochemical phenomena.

Source: PubChem (NCBI) · compound 2771