BK21 Program of Bio-Molecular Function Seminar

 

▶ Subject : Role of astrocytic Ca2+ signals in synaptic plasticity and learning: toward an approach to develop cognitive enhancers

▶ Speaker : So-Young Lee(Department of Neuroscience Tufts University)

▶ Date : 4:00PM/July 6(Wed)/2011

▶ Place : #104, Life Science Bldg.

 

*Abstract
Synapses are increasingly recognized to be tripartite structures, pre- and post-synaptic neurons and surrounding astrocytes, in which astrocytes actively modulate synaptic activity. Astrocytes respond to synaptic activity with Ca2+ elevations, and this leads to the release of gliotransmitters, such as glutamate.
Metabotropic glutamate receptor 5 (mGluR5) is receiving attention as a therapeutic target in schizophrenia since positive allosteric modulators (PAMs) of this receptor augment synaptic plasticity and cognition. It has been suggested that astrocytic Ca2+ signaling can be a source of glutamate. To determine the importance of this glial pathway in contributing to effects of mGluR5 PAMs, we used two lines of transgenic mice to activate astrocytic Gq/Ca2+ signaling or attenuate astocytic IP3-dependent Ca2+ signaling. We demonstrate that glial Ca2+ signals differentially modulate synaptic plasticity in various stimulus conditions. Notably, stimulation of astrocytic Ca2+ signaling enhances threshold long-term potentiation (LTP), which requires mGluR5 activation. The ability of mGluR5 PAMs to enhance LTP and learning requires astrocytic Ca2+ signals, raising the potential for novel astrocytic targets for cognitive enhancement in disorders such as schizophrenia.

☎ Inquiry : Kyong Tai Kim(279-2297)