[Abstract Title]. - Society for Neuroscience

Poster
242. Glial Neuronal Interactions: Glutamate and Calcium
Time: Sunday, November 16, 2008, 1:00 pm - 5:00 pm
Program#/Poster#: 242.20/J3
Topic: B.11.a. Synapses
Support: Swedish Research Council. Proj. 01580 and 12600.
Title: Astrocyte-mediated negative feedback at hippocampal glutamatergic synapses
Authors: *M. S. ANDERSSON, E. HANSE;
Neurosci & Physiol, Gothenburg Univ., Gothenburg, Sweden
Abstract: Presynaptic terminals express receptors whose activation modulates the release
probability.
These receptors can be activated by gliotransmitters and we have recently described an astrocytemediated
transient heterosynaptic depression (tHeSD) in the CA1 area of rat hippocampal slices.
A 3-impulse 50 Hz conditioning burst produces a 25% reduction in release probability of
neighbouring synapses within 500 ms in slices from 3 week old rats (Andersson et al, 2007).
Here we have addressed the question to what extent the synapses providing the conditioning
stimuli are affected by this transient depression. To examine this, a paired-pulse stimulus was
applied 500 ms after the conditioning burst (3 impulses, 50 Hz) to the same (homosynaptic)
synaptic input. This protocol resulted in a depression of 50 %, measured using either field
EPSPs, AMPA EPSCs or NMDA EPSCs, when comparing the 1 st response in the conditioning
3-impulse burst, with the 1 st response in the paired-pulse stimuli.
This transient homosynaptic depression (tHoSD) is mediated by astrocytes since it was blocked
by high concentrations of calcium chelator (BAPTA) delivered via the patch pipette to the
astrocytic network. In addition, the astrocyte-specific metabolic inhibitor fluoroacetate (FAC)
blocked the tHoSD. Similar to the tHeSD, the tHoSD exhibited a clear developmental profile
with only a 7% depression in slices from rats aging 6 to 11 postnatal days. Activation of several
receptors seems to contribute to the tHoSD. It was reduced by antagonists to GABAB-, kainate-
and adenosine A1- receptors.
These results show that a short burst gives rise to a previously unrecognized form of short term
plasticity - a synaptic negative feedback mediated by astrocytes.
Disclosures: M.S. Andersson , None; E. Hanse, None.