"Effect of green tea on reward learning in healthy individuals: a randomized, double-blind, placebo-controlled pilot study"
Background
Both clinical and preclinical studies revealed that regular intake of green tea reduced the prevalence of depressive symptoms, as well as produced antidepressant-like effects in rodents. Evidence proposed that disturbed reward learning has been associated with the development of anhedonia, a core symptom of depression. However, the relationship between green tea and reward learning is poorly investigated. Our goal was to test whether chronic treatment with green tea in healthy subjects affects the process of reward learning and subsequently regulates the depressive symptoms.
Methods
Seventy-four healthy subjects participated in a double-blind, randomized placebo-controlled study with oral administration of green tea or placebo for 5weeks. We used the monetary incentive delay task to evaluate the reward learning by measurement of the response to reward trial or no-reward trial. We compared the reaction time of reward responsiveness between green tea and placebo treatment. Furthermore, we selected Montgomery-Asberg depression rating scale (MADRS) and 17-item Hamilton Rating Scale for Depression (HRSD-17) to estimate the depressive symptoms in these two groups.
Results
The results showed chronic treatment of green tea increased reward learning compared with placebo by decreasing the reaction time in monetary incentive delay task. Moreover, participants treated with green tea showed reduced scores measured in MADRS and HRSD-17 compared with participants treated with placebo.
Conclusions
Our findings reveal that chronic green tea increased the reward learning and prevented the depressive symptoms. These results also raised the possibility that supplementary administration of green tea might reverse the development of depression through normalization of the reward function.
Keywords: Green tea, Depression, Reward learning, Anhedonia
2. "Green Tea Intake Improves Reward Learning and Symptoms of Depression"
3. "Green Tea (Camellia sinensis) Potentiates Haloperidol – Induced Extrapyr- amidal Symptoms and Decreases Dopamine Metabolism in the Dorsal Striatum of Rats"
An increase in sensitivity of DA D2 receptors has been reported fowling long term administration of Haloperidol. D2 receptors are intensely distributed both presynaptically and postsynaptically in striatal dopaminergic neurons [29, 30] and it is more likely that GTE has presynaptic and postsynaptic role in processing and integrating incoming input in nucleus accumbens (AcN) but not towards caudate putamen (CPu) of the basal ganglion network. It will be interesting to find out GTE role in pre and post synaptic events. Our results (Figs. 3 and 4) showed the effect of haloperidol on DOAPC levels tend to induce large fraction of DA catabolism occur intraneuronally in the ventral striatum. On the other hand an increase level of HVA was also observed in AcN but not in the CPu at repeated dose haloperidol and GTE intake in rats. That is explicable in
terms of increase DA release and obstructs respectively in these brain regions [32]. However the effects on ventral striatum are known to be involved in the emotional control. Haloperidol produce effects on the ventral striatum and substantia Nigra [34], impression that GTE+ HAL enhances the DA and its metabolites levels in ventral striatum may have some impact on mood modification. Recent findings have proven that motor deficits can be reduced with L- arginine (a NO donor) in dose dependent manners and demonstrated as a possible therapeutic option to reverse VCMs and increased dopamine levels [10]. It is also well documented that GTE polyphenols are a good scavenger of NO ions [32], Epigalocatechin-3-gallate (EGCG) has proven selective inhibitor of inducible nitric oxide synthase ( iNOS) in human chondrocytes [33]. Polyphenols of GTE have been shown to decrease plasma nitrite levels significantly via reversed L-arginine effects, inhibited NO production favoring antinociceptive effect in rodent [34 -35] and NO may enhance oxidative stress in entire dorsal striatum of the brain intensify motor impairment ."