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Göteborgs universitets publikationer

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

Författare och institution:
My Andersson (Institutionen för neurovetenskap och fysiologi, sektionen för fysiologi); Fredrik Blomstrand (Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap och rehabilitering); Eric Hanse (Institutionen för neurovetenskap och fysiologi, sektionen för fysiologi)
Publicerad i:
The Journal of physiology, 585 ( Pt 3 ) s. 843-52
Artikel, refereegranskad vetenskaplig
Sammanfattning (abstract):
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.
Ämne (baseras på Högskoleverkets indelning av forskningsämnen):
Medicinska grundvetenskaper ->
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
Postens nummer:
Posten skapad:
2008-10-15 09:19
Posten ändrad:
2010-01-26 12:48

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