In addition to its role as neurotransmitter, 5-HT exerts morphogenic actions and controls neurodevelopmental processes such as neurogenesis, axon guidance, dendritogenesis, synaptogenesis, cell migration and brain wiring [26, 27]. The 5-HT7R has become a promising target for the treatment of neuropsychiatric and neurologic disorders; this is evidenced by the numerous 5-HT7R antagonist drug discovery programs across the world [14]. Increasing data regarding the expression profiles of 5-HT7R show that it contributes to the establishment and remodeling of neuronal cytoarchitecture during brain development. Therefore, dysfunction or modulation of 5-HT7R is linked to the pathogenesis/pathophysiology of neurodevelopmental disorders. In the adult, 5-HT7R stimulates synaptic plasticity which, in turn, affects many physiological functions such as learning, memory, mood and reward. Therefore, the 5-HT7R is also a target in the adult, as it could influence mood disorders, schizophrenia, and other cognitive disturbance disorders [28, 29 , 30]. However, the pharmacological and genetic manipulation of 5-HT7R in animal models of depression, anxiety, schizophrenia, neuropathic pain has often given inconsistent or conflicting results. Experimental conditions such as difference in animal’s strain, behavioral tests, drugs and their doses, route of administration as well as the use of non-selective drugs have to be taken in consideration. A new level of complexity is added with the notion of biased ligands which could affect transmission and intracellular signaling systems in a different way from classical ligands. Biased agonism of test drugs could account, at least in part, for these discordant results. By gathering experts and information around these results/studies, the proposed consortium aims to understand the basis of these complexities and provided a clearer path forward by working together.