Augmentation by citalopram of risperidone-induced monoamine release in rat prefrontal cortex

Abstract

The results suggest that the ability of atypical APDs to augment the therapeutic efficacy of SSRIs in major depression and treatment-resistant depression may be due, at least in part, to potentiation of SSRI-induced increases in cortical DA and NE. The contributions of 5-HT1A receptor stimulation and 5-HT2A and alpha2 adrenergic receptor antagonism to this augmentation are discussed.

Augmentation effect of combination therapy of aripiprazole and antidepressants on forced swimming test in mice

“…Nonetheless, a recent microdialysis study in rats has demonstrated that extracellular levels of DA measured in the frontal cortex were not significantly modified after a 30-min FST session (Nakasato et al 2008). Similarly, it has been demonstrated that SSRIs (citalopram and fluvoxamine) did not affect extracellular DA levels in the frontal cortex of rats (Huang et al 2006;Ago et al 2005). In contrast, it has been demonstrated that aripiprazole produces a significant increase in extracellular levels of DA in the mouse frontal cortex Zocchi et al (2005).…”

The cannabinergic system is implicated in the upregulation of central NGF protein by psychotropic drugs

“…It can be observed from the Table 5 that both citalopram and risperidone elevated eCB contents in the frontal cortex, hippocampus, and amygdala. This may provide further justifying reason for adding citalopram to risperidone in major depression, treatment-resistant depression, or negative symptoms of schizophrenia providing long-term efficacy (Huang et al 2006;Shelton 2006). In general, brain regional distribution of endocannabinoids following psychotropic treatment suggests that the cannabinergic system may be integral to the development and maintenance of effective coping strategies to the emotional responses as well as achievement a better drug efficacy.…”

Measuring Endogenous 5-HT Release by Emission Tomography: Promises and Pitfalls

“…Unfortunately, the well-validated method of acute tryptophan depletion does not seem to produce sufficient changes in 5-HT to be visualised by currently available radiotracers (Table 2). Alternative options in humans are somewhat limited: 5-HTP and tryptophan could be used intravenously (Charig et al, 1986;den Boer and Westenberg, 1990) or further 5-HT elevation might be achieved safely by introducing augmenting agents to SSRIs, such as pindolol (Pinborg et al, 2004), ketanserin (Cremers et al, 2004;Udo de Haes et al, 2005), or risperidone (Huang et al, 2006), with antiemetic administration at higher doses to avoid nausea and caution over possible drug interactions and serotonin syndrome.…”