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Publication Detail
Short- and long-term depression at glutamatergic synapses on hippocampal interneurons by group I mGluR activation.
  • Publication Type:
    Journal article
  • Publication Sub Type:
    Journal Article
  • Authors:
    Le Duigou C, Holden T, Kullmann DM
  • Publication date:
    04/2011
  • Pagination:
    748, 756
  • Journal:
    Neuropharmacology
  • Volume:
    60
  • Issue:
    5
  • Status:
    Published
  • Country:
    England
  • PII:
    S0028-3908(10)00350-3
  • Language:
    eng
  • Keywords:
    Animals, Calcium Channels, Excitatory Amino Acid Agonists, Excitatory Postsynaptic Potentials, Glycine, Hippocampus, Interneurons, Methoxyhydroxyphenylglycol, Neuronal Plasticity, Rats, Rats, Sprague-Dawley, Receptors, Metabotropic Glutamate, Resorcinols, Signal Transduction, Synapses, Synaptic Transmission
Abstract
Group I metabotropic glutamate receptors (mGluRs) are expressed by many interneurons of the hippocampus. Although they have been implicated in short- and long-term synaptic plasticity of glutamatergic transmission, their roles in modulating transmission to interneurons are incompletely understood. The selective group I mGluR agonist (S)-3,5-dihydroxyphenylglycine (DHPG) acutely depressed transmission at synapses in the feed-forward inhibitory pathway made by Schaffer collaterals on interneurons in the rat hippocampal CA1 sub-field. DHPG elicited a qualitatively similar depression at synapses made by pyramidal neuron axon collaterals on interneurons in the feedback circuit in stratum oriens. Selective blockers revealed a link from mGluR1 to reversible, and mGluR5 to long-lasting, depression. The acute DHPG-induced depression was consistently accompanied by an elevation in paired-pulse ratio, implying a presynaptic decrease in release probability. However, it was also attenuated by blocking G-protein and Ca(2+) signalling within the postsynaptic neuron, arguing for a retrograde signalling cascade. The DHPG-evoked depression was unaffected by antagonists of CB1 and GABA(B) receptors but was occluded when presynaptic P/Q-type Ca(2+) channels were blocked. Finally, high-frequency stimulation delivered to an independent conditioning pathway evoked a heterosynaptic reversible depression, which was sensitive to group I mGluR antagonists. Group I mGluRs thus powerfully modulate synaptic excitation of hippocampal interneurons and mediate inter-synaptic cross-talk. This article is part of a Special Issue entitled 'Synaptic Plasticity & Interneurons'.
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