Classical and rapid-acting antidepressants increase TRKB turnover in dendritic spines

Show simple item record

dc.contributor Helsingin yliopisto, Bio- ja ympäristötieteellinen tiedekunta, Bio- ja ympäristötieteellinen tiedekunta fi
dc.contributor University of Helsinki, Faculty of Biological and Environmental Sciences, Faculty of Biological and Environmental Sciences en
dc.contributor Helsingfors universitet, Bio- och miljövetenskapliga fakulteten, Bio- och miljövetenskapliga fakulteten sv
dc.contributor.author Moliner, Rafael
dc.date.issued 2019
dc.identifier.uri URN:NBN:fi:hulib-201909273550
dc.identifier.uri http://hdl.handle.net/10138/305791
dc.description.abstract Classical and rapid-acting antidepressant drugs have been shown to reinstate juvenile-like plasticity in the adult brain, allowing mature neuronal networks to rewire in an environmentally-driven/activity-dependent process. Indeed, antidepressant drugs gradually increase expression of brain-derived neurotrophic factor (BDNF) and can rapidly activate signaling of its high-affinity receptor TRKB. However, the exact mechanism of action underlying drug-induced restoration of juvenile-like plasticity remains poorly understood. In this study we first characterized acute effects of classical and rapid-acting antidepressant drugs on the interaction between TRKB and postsynaptic density (PSD) proteins PSD-93 and PSD-95 in vitro. PSD proteins constitute the core of synaptic complexes by anchoring receptors, ion channels, adhesion proteins and various signaling molecules, and are also involved in protein transport and cell surface localization. PSD proteins have in common their role as key regulators of synaptic structure and function, although PSD-93 and PSD-95 are associated with different functions during development and have opposing effects on the state of plasticity in individual synapses and neurons. Secondly, we investigated changes in mobility of TRKB in dendritic structures in response to treatment with antidepressant drugs in vitro. We found that antidepressant drugs decrease anchoring of TRKB with PSD-93 and PSD-95, and can rapidly increase TRKB turnover in dendritic spines. Our results contribute to the mechanistic model explaining drug-induced restoration of juvenile-like neuronal plasticity, and may provide a common basis for the effects of antidepressant drugs. en
dc.language.iso eng
dc.publisher Helsingin yliopisto fi
dc.publisher University of Helsinki en
dc.publisher Helsingfors universitet sv
dc.subject depression en
dc.subject antidepressant en
dc.subject rapid-acting en
dc.subject plasticity en
dc.subject neurotrophin en
dc.subject BDNF en
dc.subject TRKB en
dc.subject PSD-93 en
dc.subject PSD-95 en
dc.subject iPlasticity en
dc.subject fluoxetine en
dc.subject ketamine en
dc.subject anchoring en
dc.subject interaction en
dc.subject uncoupling en
dc.subject disruption en
dc.subject synaptic complex en
dc.subject trafficking en
dc.subject dendrite en
dc.subject spine en
dc.subject synapse en
dc.title Classical and rapid-acting antidepressants increase TRKB turnover in dendritic spines en
dc.type.ontasot pro gradu -tutkielmat fi
dc.type.ontasot master's thesis en
dc.type.ontasot pro gradu-avhandlingar sv
dc.subject.discipline fysiologia ja neurotiede fi
dc.subject.discipline Physiology and Neuroscience en
dc.subject.discipline fysiologi och neurovetenskap sv
dct.identifier.urn URN:NBN:fi:hulib-201909273550

Files in this item

Files Size Format View
Moliner_Rafael_pro_gradu_2019.pdf 2.593Mb application/pdf View/Open

This item appears in the following Collection(s)

Show simple item record