[Abstract Title]. - Society for Neuroscience

Program#/Poster#: 242.5/H12
Topic: B.11.a. Synapses
Support: NIMH
NINDS
Title: Astrocytes promote synaptic plasticity by activating mGluR5
Authors: *S.-Y. LEE 1 , M. M. HALASSA 1 , O. PASCUAL 2 , P. G. HAYDON 1 ;
1 Univ. Pennsylvania, Philadelphia, PA; 2 Biologie Cellulaire de la Synapse, INSERM, Paris,
France
Abstract: Though electrically non-excitable, astrocytes respond to external signals by an
increase in intracellular Ca 2+ . Astrocytic Ca 2+ signaling can result in a number of physiological
consequences, including the release of chemical transmitters from these cells, to impact nearby
neuronal activity. The role of astrocytic Ca 2+ signaling in synaptic transmission and plasticity,
however, remains poorly understood. Here, we show that elevating Ca 2+ selectively in astrocytes
using photolysis of the Ca 2+ cage o-nitrophenyl-EGTA in area CA1 of the hippocampus triggers
two forms of plasticity; long-term facilitation (LTF) and long-term depression (LTD). Whether a
neuron exhibited LTF or LTD was dependent on its membrane potential at the time of astrocytic
activation; elevation of astrocytic Ca 2+ coincident with neuronal depolarization resulted in LTF
while coincidence with neuronal hyperpolarization resulted in LTD. Both forms of plasticity
were dependent on metabotropic glutamate receptor 5 (mGluR5) while LTF was also dependent
on NMDA receptor activity. To test whether astrocytic Ca 2+ signaling was necessary for known
forms of plasticity in the hippocampus, we generated a transgenic animal in which IP3 5phosphatase
was selectively and conditionally expressed in astrocytes to attenuate IP3-dependent
Ca 2+ signaling. Transgenic inhibition of astrocytic Ca 2+ signaling resulted in attenuated Schaffer
collateral-CA1 long-term potentiation (LTP). This transgenic phenotype was mimicked by
dialysis of the Ca 2+ chelator BAPTA into the astrocytic syncytium to attenuate activitydependent
astrocytic Ca 2+ signaling. These results demonstrate that astrocytic Ca 2+ signaling,
which is recruited by neuronal activity, is required for synaptic plasticity.
Disclosures: S. Lee , None; M.M. Halassa, None; O. Pascual, None; P.G. Haydon, None.
Poster
242. Glial Neuronal Interactions: Glutamate and Calcium
Time: Sunday, November 16, 2008, 1:00 pm - 5:00 pm
Program#/Poster#: 242.6/I1