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The Journal of Neuroscience, February 28, 2007, 27(9):2261-2271; doi:10.1523/JNEUROSCI.5582-06.2007

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Cellular/Molecular
Parvalbumin Is a Mobile Presynaptic Ca²⁺ Buffer in the Calyx of Held that Accelerates the Decay of Ca²⁺ and Short-Term Facilitation

Martin Müller,^1,2 Felix Felmy,³ Beat Schwaller,⁴ and Ralf Schneggenburger¹

¹Laboratory of Synaptic Mechanisms, Brain-Mind Institute, École Polytechnique Fédérale de Lausanne, 1015 Lausanne, Switzerland, ²Graduate School of Neural and Behavioral Sciences, Universität Tübingen, 72074 Tübingen, Germany, ³Biology II, Department for Neurobiology, Ludwig-Maximilians-University, 82152 Martinsried, Germany, and ⁴Unit of Anatomy, Department of Medicine, University of Fribourg, 1705 Fribourg, Switzerland

Correspondence should be addressed to Dr. Ralf Schneggenburger, Laboratory of Synaptic Mechanisms, École Polytechnique Fédérale de Lausanne, Brain Mind Institute, Bâtiment AAB, Station 15, CH-1015 Lausanne, Switzerland. Email: ralf.schneggenburger{at}epfl.ch

Presynaptic Ca²⁺ signaling plays a crucial role in short-term plasticity of synaptic transmission. Here, we studied the role of mobile endogenous presynaptic Ca²⁺ buffer(s) in modulating paired-pulse facilitation at a large excitatory nerve terminal in the auditory brainstem, the calyx of Held. To do so, we assessed the effect of presynaptic whole-cell recording, which should lead to the diffusional loss of endogenous mobile Ca²⁺ buffers, on paired-pulse facilitation and on intracellular Ca²⁺ concentration ([Ca²⁺]_i) transients evoked by action potentials. In unperturbed calyces briefly preloaded with the Ca²⁺ indicator fura-6F, the [Ca²⁺]_i transient decayed surprisingly fast (_fast, 30 ms). Presynaptic whole-cell recordings made without additional Ca²⁺ buffers slowed the decay kinetics of [Ca²⁺]_i and paired-pulse facilitation (twofold to threefold), but the amplitude of the [Ca²⁺]_i transient was changed only marginally. The fast [Ca²⁺]_i decay was restored by adding the slow Ca²⁺ buffer EGTA (50–100 µM) or parvalbumin (100 µM), a Ca²⁺-binding protein with slow Ca²⁺-binding kinetics, to the presynaptic pipette solution. In contrast, the fast Ca²⁺ buffer fura-2 strongly reduced the amplitude of the [Ca²⁺]_i transient and slowed its decay, suggesting that the mobile endogenous buffer in calyces of Held has slow, rather than fast, binding kinetics. In parvalbumin knock-out mice, the decay of [Ca²⁺]_i and facilitation was slowed approximately twofold compared with wild-type mice, similar to what is observed during whole-cell recordings in rat calyces of Held. Thus, in young calyces of Held, a mobile Ca²⁺ buffer with slow binding kinetics, primarily represented by parvalbumin, accelerates the decay of spatially averaged [Ca²⁺]_i and paired-pulse facilitation.

Key words: synaptic transmission; Ca²⁺; facilitation; short-term plasticity; Ca²⁺-binding protein; nerve terminal

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Received June 7, 2006; revised Jan. 24, 2007; accepted Jan. 24, 2007.

Correspondence should be addressed to Dr. Ralf Schneggenburger, Laboratory of Synaptic Mechanisms, École Polytechnique Fédérale de Lausanne, Brain Mind Institute, Bâtiment AAB, Station 15, CH-1015 Lausanne, Switzerland. Email: ralf.schneggenburger{at}epfl.ch

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