Although the interaction between the BNDF and 5-HT provides a promising bridge between structural and functional neuronal activity, and serves as explanatory hypothesis for neuronal plasticity deficits in neuropsychiatric disorders, exact mechanisms underlying the regulation of the cross connection between BDNF and 5-HT in humans remain unresolved. Our data in concert with above referred work speak for a similar expression of 5-HTT and 5HT1A receptors upon life-time BDNF reduction, but unfortunately do not illuminate the mechanisms leading to this observation. Theoretically, counter-regulatory or compensatory effects may have altered 5-HTT and 5-HT1A expression. Furthermore, it is possible that not absolute numbers but functional activity of serotonergic structures is altered by BDNF. The evidence on connections between depression and BNDF genotype status is inconsistent as well. Meta-analytical research suggested an association of Val66Met with major depressive disorder antidepressant treatment response or hippocampal volume and a role of gender and ethnicity. However, recent meta-analyses refuted these associations and detected power deficits in many trials. Low serum levels of BDNF were suggested as potential peripheral marker of depression and increase of serum BDNF as response to the appropriate first-line treatment with selective 5-HT reuptake inhibitors. Likewise, this association is weaker than initially thought and there is no relationship between symptom severity and BDNF serum concentration. Our results suggest no association between allelic distribution and diagnosis. Our small number of MDD subjects remain a limiting factor in that Rhynchophylline regard. Unfortunately a common problem of human PET studies is weak power resulting from low subject numbers, owed to the large effort of conducting PET-imaging. This is even more intrinsic to genetic PET studies reporting results based on genotype subgroups and in SNP neuroimaging studies where pooling of rare genotype groups is common practice. The low subject number in the MDD met-carrier group could therefore be a Wilforlide-A limitation of our study.