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This Article Full Text Full Text (PDF) All Versions of this Article: 573/1/65    most recent jphysiol.2005.103770v1 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 Canepari, M. Articles by Ogden, D. Search for Related Content PubMed PubMed Citation Articles by Canepari, M. Articles by Ogden, D. Related Collections Neuroscience

¹ National Institute for Medical Research, London NW7 1AA, UK
² Laboratoire de Physiologie Cérébrale UMR8118 Université Paris 5, Paris 75006, France

Type 1 metabotropic glutamate receptors (mGluR1) in Purkinje neurones (PNs) are important for motor learning and coordination. Here, two divergent mGluR1 Ca²⁺-signalling pathways and the associated membrane conductances were distinguished kinetically and pharmacologically after activation by 1-ms photorelease of L-glutamate or by bursts of parallel fibre (PF) stimulation. A new, mGluR1-mediated transient K⁺ conductance was seen prior to the slow EPSC (sEPSC). It was seen only in PNs previously allowed to fire spontaneously or held at depolarized potentials for several seconds and was slowly inhibited by agatoxin IVA, which blocks P/Q-type Ca²⁺ channels. It peaked in 148 ms, had well-defined kinetics and, unlike the sEPSC, was abolished by the phospholipase C (PLC) inhibitor U73122. It was blocked by the BK Ca²⁺-activated K⁺ channel blocker iberiotoxin and unaffected by apamin, indicating selective activation of BK channels by PLC-dependent store-released Ca²⁺. The K⁺ conductance and underlying transient Ca²⁺ release showed a highly reproducible delay of 99.5 ms following PF burst stimulation, with a precision of 1–2 ms in repeated responses of the same PN, and a subsequent fast rise and fall of Ca²⁺ concentration. Analysis of Ca²⁺ signals showed that activation of the K⁺ conductance by Ca²⁺ release occured in small dendrites and subresolution structures, most probably spines. The results show that PF burst stimulation activates two pathways of mGluR1 signalling in PNs. First, transient, PLC-dependent Ca²⁺ release from stores with precisely reproducible timing and second, slower Ca²⁺ influx in the cation-permeable sEPSC channel. The priming by prior Ca²⁺ influx in P/Q-type Ca²⁺ channels may determine the path of mGluR1 signalling. The precise timing of PLC-mediated store release may be important for interactions of PF mGluR1 signalling with other inputs to the PN.

(Received 22 December 2005; accepted after revision 21 February 2006; first published online 23 February 2006)
Corresponding author D. Ogden: National Institute for Medical Research, Mill Hill, London NW7 1AA, UK. Email: dogden{at}nimr.mrc.ac.uk

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