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This Article Full Text Full Text (PDF) All Versions of this Article: 575/1/115    most recent jphysiol.2006.112896v1 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 Topolnik, L. Articles by Lacaille, J.-C. Search for Related Content PubMed PubMed Citation Articles by Topolnik, L. Articles by Lacaille, J.-C. Related Collections Neuroscience

¹ Département de Physiologie, Centre de Recherche en Sciences Neurologiques, Université de Montréal, Case Postale 6128, Succursale Centre-Ville, Montréal, Qc, Canada H3C 3J7

Hippocampal inhibitory interneurones demonstrate pathway- and synapse-specific rules of transmission and plasticity, which are key determinants of their role in controlling pyramidal cell excitability. Mechanisms underlying long-term changes at interneurone excitatory synapses, despite their importance, remain largely unknown. We use two-photon calcium imaging and whole-cell recordings to determine the Ca²⁺ signalling mechanisms linked specifically to group I metabotropic glutamate receptors (mGluR1 and mGluR5) and their role in hebbian long-term potentiation (LTP) in oriens/alveus (O/A) interneurones. We demonstrate that mGluR1 activation elicits dendritic Ca²⁺ signals resulting from Ca²⁺ influx via transient receptor potential (TRP) channels and Ca²⁺ release from intracellular stores. By contrast, mGluR5 activation produces dendritic Ca²⁺ transients mediated exclusively by intracellular Ca²⁺ release. Using Western blot analysis and immunocytochemistry, we show mGluR1-specific extracellular signal-regulated kinase (ERK1/2) activation via Src in CA1 hippocampus and, in particular, in O/A interneurones. Moreover, we find that mGluR1/TRP Ca²⁺ signals in interneurone dendrites are dependent on activation of the Src/ERK cascade. Finally, this mGluR1-specific Ca²⁺ signalling controls LTP at interneurone synapses since blocking either TRP channels or Src/ERK and intracellular Ca²⁺ release prevents LTP induction. Thus, our findings uncover a novel molecular mechanism of interneurone-specific Ca²⁺ signalling, critical in regulating synaptic excitability in hippocampal networks.

(Received 3 May 2006; accepted after revision 30 May 2006; first published online 1 June 2006)
Corresponding author J.-C. Lacaille: Département de Physiologie, Centre de Recherche en Sciences Neurologiques, Université de Montréal, Case Postale 6128, Succursale Centre-Ville, Montréal, Qc, Canada H3C 3J7. Email: jean-claude.lacaille{at}umontreal.ca

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