Thereby, BDNF is a major factor in the proper development and plastic regulation of the central nervous system and highly active in limbic structures such as the hippocampus and the amygdala, where long-term potentiation, learning and memory are facilitated. However, it should be stated here that most of the evidence of BDNF in this context is based on rodent data. The BDNF gene is located at chromosome 11p13-14, including many splice sites and promoters. All BDNF mRNAs are initially translated into proBDNF and are then cleaved into mature BDNF. The most investigated polymorphism of the BDNF gene exists in the codon 66 of proBDNF and consists of a valine to methionine substitution, which is associated with reduced intracellular proBDNF trafficking, synaptic secretion of BDNF, and thus a lower extracellular BDNF concentration in met-allele carriers. Thought to trigger deficits in neuronal development and plasticity, the Val66Met polymorphism is of major interest in Salvianolic-acid-B neuropsychiatric research. Interestingly, in humans the molecular connections between 5HT and BDNF, and how alterations in one system affect the other are hardly known. Due to the lack of current methods to measure BDNF, TrkB or p75 in the living human brain, in vivo research in humans mainly focuses on the investigation of alterations of serotonergic structures thought to be mediated via changes in BDNF. In imaging genetics studies, serotonergic markers are labeled by radioligands and their binding is measured using PET. As yet, there exist three studies investigating alterations of BDNF, as represented by the Val66Met polymorphism, and it��s association with binding of 5-HT1A, 5-HT2A receptors as well as the 5HTT in the human brain. Two previous studies failed to detect links between Val66Met and binding of Forsythoside-A 5-HT1A and 5HT2A receptors. On the other side, a recently published study reports lower 5-HT1A binding in healthy subjects carrying the met-allele compared to val-homozygotes, a difference which was not observed in depressed subjects.As far as 5-HTT is concerned, in one study, applying the serotonin transporter specific radioligand MADAM with PET and -?-CIT with single photon emission tomography in two independent samples, the authors found increased 5-HTT binding in val-homozygote male subjects and compared to met-allele carriers.