File Download

There are no files associated with this item.

Conference Paper: Elucidating how cyclin-dependent kinase 5 (Cdk5) regulates synapse function in neuron

TitleElucidating how cyclin-dependent kinase 5 (Cdk5) regulates synapse function in neuron
Authors
Issue Date2014
Citation
The 2014 Physiology Symposium and Joint Scientific Conference of the Hong Kong Society of Neurosciences (HKSN) and the Biophysical Society of Hong Kong, Hong Kong, 12-14 June 2014. How to Cite?
AbstractOur brain function depends on communication between neurons through synaptic transmission. Most excitatory synapses are located on specialized protrusions on the dendrites called dendritic spines, which have heterogeneous morphologies and are highly dynamic. The stability and morphology of dendritic spines can be regulated by synaptic activity and specific growth factors such as the neurotrophin BDNF. This activity-dependent spine morphogenesis is a crucial mechanism by which experience modulates the efficacy of synaptic transmission, and is fundamental to brain development and function such as memory formation. Indeed, altered spine density and morphology is associated with neurodevelopmental disorders including intellectual disability and autism. Delineating the molecular mechanisms that underlie dendritic spine development and remodeling might therefore provide important insights into the molecular basis of various mental disorders. Spine growth and remodeling requires changes in actin cytoskeleton, gene transcription and protein synthesis that involve multiple signaling cascades regulated through protein phosphorylation. Emerging evidence suggests that the serine/threonine kinase Cdk5 is critically involved in regulating synapse function and synaptic plasticity, but the underlying mechanisms remain elusive. Here I will describe the function of Cdk5 in promoting dendritic spine morphogenesis via phosphorylation of the BDNF receptor TrkB and the signaling protein S6 kinase (p70S6K1). Through identification of the major phosphorylation sites and generation of phospho-deficient mutants, the importance of Cdk5-mediated phosphorylation of TrkB and p70S6K1 in activity-dependent spine plasticity and maturation will be discussed.
Persistent Identifierhttp://hdl.handle.net/10722/206030

 

DC FieldValueLanguage
dc.contributor.authorLai, KOen_US
dc.date.accessioned2014-10-20T11:29:34Z-
dc.date.available2014-10-20T11:29:34Z-
dc.date.issued2014en_US
dc.identifier.citationThe 2014 Physiology Symposium and Joint Scientific Conference of the Hong Kong Society of Neurosciences (HKSN) and the Biophysical Society of Hong Kong, Hong Kong, 12-14 June 2014.en_US
dc.identifier.urihttp://hdl.handle.net/10722/206030-
dc.description.abstractOur brain function depends on communication between neurons through synaptic transmission. Most excitatory synapses are located on specialized protrusions on the dendrites called dendritic spines, which have heterogeneous morphologies and are highly dynamic. The stability and morphology of dendritic spines can be regulated by synaptic activity and specific growth factors such as the neurotrophin BDNF. This activity-dependent spine morphogenesis is a crucial mechanism by which experience modulates the efficacy of synaptic transmission, and is fundamental to brain development and function such as memory formation. Indeed, altered spine density and morphology is associated with neurodevelopmental disorders including intellectual disability and autism. Delineating the molecular mechanisms that underlie dendritic spine development and remodeling might therefore provide important insights into the molecular basis of various mental disorders. Spine growth and remodeling requires changes in actin cytoskeleton, gene transcription and protein synthesis that involve multiple signaling cascades regulated through protein phosphorylation. Emerging evidence suggests that the serine/threonine kinase Cdk5 is critically involved in regulating synapse function and synaptic plasticity, but the underlying mechanisms remain elusive. Here I will describe the function of Cdk5 in promoting dendritic spine morphogenesis via phosphorylation of the BDNF receptor TrkB and the signaling protein S6 kinase (p70S6K1). Through identification of the major phosphorylation sites and generation of phospho-deficient mutants, the importance of Cdk5-mediated phosphorylation of TrkB and p70S6K1 in activity-dependent spine plasticity and maturation will be discussed.en_US
dc.languageengen_US
dc.relation.ispartofPhysiology Symposium & Joint Scientific Conference of the Hong Kong Society of Neurosciences & the Biophysical Society of Hong Kongen_US
dc.titleElucidating how cyclin-dependent kinase 5 (Cdk5) regulates synapse function in neuronen_US
dc.typeConference_Paperen_US
dc.identifier.emailLai, KO: laiko@hku.hken_US
dc.identifier.authorityLai, KO=rp01891en_US
dc.identifier.hkuros240825en_US

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats