Summary: SSRI's, ketamine, and tricyclic antidepressants all bind with TrkB.The findings challenge the roles serotonin and glutamate receptors play in the effects of antidepressant medications. Source: University of Helsinki The effects of selective serotonin reuptake inhibitors (SSRIs) and other conventional antidepressants are believed to be based on their increasing the levels of

Endogenous cognate ligands for Trk receptors are homodimers, which can only selectively bind to one of the Trk receptors, whereas amitriptyline binds to both TrkA and TrkB receptors, leading to a heterodimer formation. Hence, this discovery establishes a proof-of-concept model for identifying small molecular agonists and antagonists for RTK.

The functional trkB-selective antibodies showed distinct pharmacological profiles, ranging from partial agonists to antagonists, acting on trkB receptors through allosteric modulations. The same diversity of effects was observed on the mitogen-activated protein kinase signalling pathway downstream of trkB and on the subsequent neurite outgrowth.

Summary: SSRI's, ketamine, and tricyclic antidepressants all bind with TrkB.The findings challenge the roles serotonin and glutamate receptors play in the effects of antidepressant medications. Source: University of Helsinki The effects of selective serotonin reuptake inhibitors (SSRIs) and other conventional antidepressants are believed to be based on their increasing the levels of

Endogenous cognate ligands for Trk receptors are homodimers, which can only selectively bind to one of the Trk receptors, whereas amitriptyline binds to both TrkA and TrkB receptors, leading to a heterodimer formation. Hence, this discovery establishes a proof-of-concept model for identifying small molecular agonists and antagonists for RTK.

The functional trkB-selective antibodies showed distinct pharmacological profiles, ranging from partial agonists to antagonists, acting on trkB receptors through allosteric modulations. The same diversity of effects was observed on the mitogen-activated protein kinase signalling pathway downstream of trkB and on the subsequent neurite outgrowth.