Dynamics of Ca2+ and Na+ in the dendrites of mouse cerebellar Purkinje cells evoked by parallel fibre stimulation

Authors

  • Akinori Kuruma,

    1. Laboratory for Developmental Neurobiology, Brain Science Institute, RIKEN, 2–1 Hirosawa, Wako, Saitama, 351–0198 Japan
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  • Takafumi Inoue,

    1. Division of Molecular Neurobiology, The Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo, 108–8639 Japan
    2. Calcium Oscillation Project, ICORP, Japan Science and Technology Corporation (JST), 3-14-4 Shirokanedai, Minato-ku, Tokyo, 108–0071 Japan
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  • Katsuhiko Mikoshiba

    1. Laboratory for Developmental Neurobiology, Brain Science Institute, RIKEN, 2–1 Hirosawa, Wako, Saitama, 351–0198 Japan
    2. Division of Molecular Neurobiology, The Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo, 108–8639 Japan
    3. Calcium Oscillation Project, ICORP, Japan Science and Technology Corporation (JST), 3-14-4 Shirokanedai, Minato-ku, Tokyo, 108–0071 Japan
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: Dr Takafumi Inoue, at Division of Molecular Neurobiology, as above.
E-mail: tinoue@ims.u-tokyo.ac.jp

Abstract

Ca2+ and Na+ play important roles in neurons, such as in synaptic plasticity. Their concentrations in neurons change dynamically in response to synaptic inputs, but their kinetics have not been compared directly. Here, we show the mechanisms and dynamics of Ca2+ and Na+ transients by simultaneous monitoring in Purkinje cell dendrites in mouse cerebellar slices. High frequency parallel fibre stimulation (50 Hz, 3–50-times) depolarized Purkinje cells, and Ca2+ transients were observed at the anatomically expected sites. The magnitude of the Ca2+ transients increased linearly with increasing numbers of parallel fibre inputs. With 50 stimuli, Ca2+ transients lasted for seconds, and the peak [Ca2+] reached ∼100 µm, which was much higher than that reported previously, although it was still confined to a part of the dendrite. In contrast, Na+ transients were sustained for tens of seconds and diffused away from the stimulated site. Pharmacological interventions revealed that Na+ influx through α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors and Ca2+ influx through P-type Ca channels were essential players, that AMPA receptors did not operate as a Ca2+ influx pathway and that Ca2+ release from intracellular stores through inositol trisphosphate receptors or ryanodine receptors did not contribute greatly to the large Ca2+ transients.

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