TrkB

…pro-survival receptors TrkA, TrkB or TrkC, as well as to p75NTR death receptor. While these molecules have been shown to significantly slow or prevent neurodegeneration, their reduced bioavailability and inability to penetrate the blood-brain-barrier limit their use as potential therapeutics. To bypass these limitations, our research team has developed and patented small-sized, lipophilic

…mediated by their direct binding to TrkB. In addition, it has recently been reported that psychedelics LSD and psilocybin, also bind to TrkB with higher affinity than antidepressants. In this study, we investigated whether psychedelics and classical antidepressants promote TrkB dimerization and neurotrophic signalling in a differential manner. The effects of psychedelics on the TrkB dimerization dynamics and neurotrophic signalling associated with plasticity were studied treating N2a c

…to bind directly to BDNF receptor TrkB to promote neuronal plasticity. Like antidepressants, environmental enrichment has been shown to promote neuronal plasticity in the brain, although the exact mechanisms of action are unknown. Environmental enrichment could thus potentially act as a complementary or alternative non-pharmacological treatment for neuropsychogical disorders. This study investigated the effect of 10 weeks of environm

…levels increase and the BDNF-TRKB signaling indicate a deep interconnection between the two pathways. Moreover, chronic stress with elevated glucocorticoids levels and downregulation of TRKB signaling associated with reduced BDNF are both involved in the pathophysiology of different psychiatric disorders.In this study we investigated in vitro the molecular mechanisms underlying the interplay of glucocorticoids and TRKB signaling. We found that the glucocorticoid receptor physically interacts with TRKB, modulating its dimer

…diethylamide (LSD) directly bind to TrkB, the receptor for BDNF. Our data suggest that antidepressant and plasticity promoting-effect of psychedelics are mediated by TrkB. Our objective is to test in vivo the effect of LSD on brain functional connectivity, more specifically on the default mode network, and the impact of the modulation of TrkB receptor on this effect. Methods. Functional Ultrasou

…Neurotrophic Factor and its receptor TrkB. Moreover, Somatostatin (SST) expressing interneurons are involved in neuronal plasticity and are important in modulating cocaine-seeking behaviour in mice.We are testing the role of TrkB in Somatostatin(SST)-expressing neurons in the formation

Background: Prenatal alcohol exposure (PAE) induces a wide range of neurodevelopmental disabilities grouped under the term fetal alcohol spectrum disorders (FASD). The effects of PAE on brain development are dependent on complex long-lasting neurochemical events, including modification of glutamate receptors. Here, we explored whether PAE may affect the functional connectivity and, further, the molecular composition of the glutamatergic synapses in the prefrontal cortex (PFC) of adolescent mice and its effect on social behaviors.Methods: We generated an in vivo model of PAE, by exposing C57Bl/

…via receptor Tyrosine Kinase B (TrkB). Impaired BDNF/TrkB signalling has been associated with several neurological disorders. A treatment with Fingolimod has been shown in vitro and in vivo to promote BDNF synthesis and release and exert BDNF-dependent neuroprotection. Estrogens are a group of steroid sex hormones synthesised by neurons and astrocytes predominantly in females. In the hippocampus, estradiol plays a cruc

…including the neurotrophin receptor TrkB. The later interaction was confirmed both in cultur

…Here, we investigated the role of BDNF-TrkB signaling in modulating the plasticity of the malignant synapse. BDNF ligand activation of its canonical receptor, TrkB (which is encoded for by the gene NTRK2),

…factor (BDNF) and its receptor TRKB are critical regulators of neuronal plasticity and have been implicated in the antidepressant action. We have recently found that many, if not all, different antidepressants, including serotonin selective SSRIs, tricyclic as well as fast-acting ketamine, directly bind to TRKB, thereby promoting TRKB translocation to synapt