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This Article Full Text Full Text (PDF) All Versions of this Article: 585/3/843    most recent jphysiol.2007.142737v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Andersson, M. Articles by Hanse, E. Search for Related Content PubMed PubMed Citation Articles by Andersson, M. Articles by Hanse, E. Related Collections Neuroscience

¹ Institute of Neuroscience and Physiology, Göteborg University, Göteborg, Sweden

Active synapses can reduce the probability of transmitter release at neighbouring synapses. Depending on whether such heterosynaptic depression is mediated by intersynaptic diffusion of transmitter or by release of gliotransmitters, astrocytes should either hinder or promote the heterosynaptic depression. In the present study we have examined the developmental profile and astrocytic involvement in a transient heterosynaptic depression (tHeSD) in the CA1 region of the rat hippocampal slice preparation. A short stimulus burst (3 impulses at 50 Hz) to one group of synapses elicited a depression of the field EPSP evoked in another group of synapses that amounted to about 25% 0.5 s after the conditioning burst. This tHeSD was associated with an increase in the paired-pulse ratio of about 30%. The tHeSD was not present in slices from rats younger than 10 postnatal days and developed towards the adult magnitude between postnatal days 10 and 20. The tHeSD was totally prevented by the glia-specific toxin fluoroacetate (FAC), by carbenoxolone, a general blocker of connexin-based channels, and by endothelin, an endogenous peptide that has been shown to block astrocytic connexin-based channels. Antagonists to GABA_B receptors and group II/III metabotropic glutamate receptors (mGluRs) abolished the tHeSD whereas antagonists to NMDA- and adenosine A1 receptors, and to group I mGluRs, did not affect the tHeSD. These results suggest that the tHeSD relies on GABA_B receptors, group II/III mGluRs and on gliotransmitter release from functionally mature astrocytes.

(Received 9 August 2007; accepted after revision 17 October 2007; first published online 25 October 2007)
Corresponding author M. Andersson: Göteborg University, Institute of Neuroscience and Physiology, Box 432, Medicinaregatan 11, 405 30 Göteborg, Sweden. Email: my.andersson{at}physiol.gu.se

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