Therefore, augmentation strategies including modifiable lifestyle behaviors, along with searching for new pharmacological treatment possibilities, are required.
The prevalence of depression is increasing, while its available treatment options do not provide satisfactory effects in a large percent of patients (Trivedi et al. It should be noted that adenosine via inhibitory A 1 and excitatory A 2A receptors regulates the release of all known neurotransmitters (Sebastião and Ribeiro 2009), which points to the role of caffeine at low, usually consumed doses in diseases associated with neurotransmitters imbalance, e.g., depression and, presumably, its treatment. In terms of the underlying mechanisms, a low dose of caffeine acts as a nonselective antagonist of adenosine acting at A 1 and A 2A adenosine receptors, while adenosine receptors are not required for the effects observed after administration of its higher doses (Fredholm et al. Low to moderate doses (50–300 mg) induce behavioral stimulation: physical endurance, reduction of fatigue, and enhancement of mental alertness and concentration, while higher doses cause aversion, irritability, and discomfort (Benowitz 1990 Heckman et al.
It is widely accepted that caffeine produces a biphasic effect. It is derived mainly from the dietary sources, i.e., coffee and tea, while its other sources include soft drinks like cola and energy drinks as well as cold medications, analgesics, and dietary supplements. Adora1, Slc6a15, and Comt may be involved in the antidepressant-like effect observed after joint administration of caffeine and mianserin or agomelatine, following chronic treatment with caffeine.Ĭaffeine (1,3,7-trimethylxanthine) is the world’s most frequently used psychoactive substance. Withdrawal of caffeine after its chronic intake can modify the activity of antidepressants. Moreover, in mice treated with caffeine for 14 days, joint administration of mianserin and caffeine on day 15 decreased adenosine A1 receptor ( Adora1) and catechol- O-methyltransferase ( Comt) mRNA level in the Cx, compared to the group which received mianserin without caffeine on this day. In mice treated with caffeine for 14 days, joint administration of agomelatine or mianserin and caffeine on day 15 decreased solute carrier family 6, member 15 ( Slc6a15), messenger RNA (mRNA) level in the Cx, compared to the group which received only the respective antidepressant on this day. Administration of agomelatine or mianserin on day 15 did not produce an antidepressant-like effect, but such effect was observed after administration of agomelatine or mianserin simultaneously with caffeine on day 15, in both mice that received saline and caffeine for 14 days. There were no changes in the immobility time between mice that received saline and caffeine for 14 days. We used the forced swim test (FST), tail suspension test (TST), and locomotor activity test in mice and quantitative real-time PCR analysis of the selected genes in the cerebral cortex (Cx). We aimed to investigate the effects of chronic treatment with caffeine (5 mg/kg, twice daily for 14 days) on the activity of single, ineffective doses of agomelatine (20 mg/kg) or mianserin (10 mg/kg) given on day 15 alone or simultaneously with caffeine. Depressed patients often present increased consumption of caffeine.
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