Effects of ketamine and N-methyl-d-aspartate on fluoxetine-induced antidepressant-related behavior using the forced swimming test

Repeated ketamine treatment induces sex-specific behavioral and neurochemical effects in mice

“…The beneficial effects of repeated ketamine treatment observed in male mice are consistent with earlier studies that have investigated the antidepressant-like effects of various repeated ketamine treatment regimens in rodents [27][28][29][30][31][32]. Of note, the adverse effects of repeated ketamine treatment observed in females fit nicely with our recent finding that a single dose of ketamine (10 mg/kg) may induce rapid sex-specific anxiety-like effects in female mice subjected to the OFT [18].…”

“…The sub-anesthetic doses of ketamine implemented and route of administration selected are commonly used to screen for the antidepressant-like effects of ketamine in preclinical rodent models [18,26]. Earlier studies have implemented similar drug regimens to investigate the antidepressant-like effects of repeated ketamine treatment in rodents [27][28][29][30][31][32] (Table 1). In an initial dose-dependent study we wondered whether male and female mice would display differential responsiveness to increasing doses of repeated ketamine treatment in the open field test (OFT) and the FST (Fig.…”

Evidence for the involvement of NMDA receptors in the antidepressant-like effect of nicotine in mouse forced swimming and tail suspension tests

“…Data showed that ketamine at the doses 3 and 1 mg/kg significantly decreased the immobility duration in the FST and TST, respectively; but at lower doses, it did not affect the immobility time. In previous studies, these doses of ketamine were also recognized as effective and non-effective doses, respectively (Cunha et al 2015;Ghasemi et al 2010;Mantovani et al 2003b;Owolabi et al 2014). MK-801 (0.1 mg/kg in the FST; 0.01 mg/kg in the TST), when administered 45 min before behavioral tests, reduced the immobility time of mice significantly, but at the dose 0.05 and 0.005 mg/kg, it did not cause significant reduction in the immobility time in FST and TST.…”

Coadministration of ketamine with conventional antidepressants in animal models of depression

“…This line of research is favorable for developing new treatments for depression with the potential to decrease much of the morbidity and mortality associated with the delayed onset of action of conventional antidepressants. [15,16] A number of studies have been published on the mechanism of antidepressant effect of ketamine. The summary of pharmacodynamics is (1) blockade of interneuronal NMDA receptors, (2) disinhibition of pyramidal cells leading to a glutamate surge, (3) activation of the AMPA receptors, (4) blockade of the excitotoxic extrasynaptic NMDA receptors, (5) activation of synaptogenic intracellular signaling and brain-derived neurotropic factor pathways, and (6) stimulation of the mammalian target of rapamycin.…”