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Astrocytes play a critical role in transient heterosynaptic depression in the rat hippocampal CA1 region.

Journal article
Authors My Andersson
Fredrik Blomstrand
Eric Hanse
Published in The Journal of physiology
Volume 585
Issue Pt 3
Pages 843-52
ISSN 0022-3751
Publication year 2007
Published at Institute of Neuroscience and Physiology, Department of Physiology
Institute of Neuroscience and Physiology, Department of Clinical Neuroscience and Rehabilitation
Pages 843-52
Language en
Keywords Animals, Astrocytes, drug effects, physiology, Electric Stimulation, Excitatory Postsynaptic Potentials, physiology, Hippocampus, cytology, growth & development, physiology, Models, Neurological, Neuroglia, drug effects, metabolism, physiology, Neuronal Plasticity, drug effects, physiology, Neurotransmitter Agents, metabolism, physiology, Rats, Rats, Wistar, Receptor, Adenosine A1, physiology, Receptors, GABA-B, physiology, Receptors, Glutamate, physiology, Receptors, N-Methyl-D-Aspartate, physiology, Synapses, drug effects, physiology
Subject categories Physiology


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.

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