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Direct modulation of synaptic vesicle priming by GABAB receptor activation at a glutamatergic synapse

Author

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  • Takeshi Sakaba

    (Max Planck Institute for Biophysical Chemistry)

  • Erwin Neher

    (Max Planck Institute for Biophysical Chemistry)

Abstract

Second messenger cascades involving G proteins1,2 and calcium3 are known to modulate neurotransmitter release4,5. A prominent effect of such a cascade is the downmodulation of presynaptic calcium influx6,7, which markedly reduces evoked neurotransmitter release5,7,8. Here we show that G-protein-mediated signalling, such as through GABA (γ-amino butyric acid) subtype B (GABAB) receptors, retards the recruitment of synaptic vesicles during sustained activity and after short-term depression. This retardation occurs through a lowering of cyclic AMP, which blocks the stimulatory effect of increased calcium concentration on vesicle recruitment. In this signalling pathway, cAMP (functioning through the cAMP-dependent guanine nucleotide exchange factor) and calcium/calmodulin cooperate to enhance vesicle priming. The differential modulation of the two forms of synaptic plasticity, presynaptic inhibition and calcium-dependent recovery from synaptic depression, is expected to have interesting consequences for the dynamic behaviour of neural networks.

Suggested Citation

  • Takeshi Sakaba & Erwin Neher, 2003. "Direct modulation of synaptic vesicle priming by GABAB receptor activation at a glutamatergic synapse," Nature, Nature, vol. 424(6950), pages 775-778, August.
    • Handle: RePEc:nat:nature:v:424:y:2003:i:6950:d:10.1038_nature01859
    DOI: 10.1038/nature01859
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    Cited by:

    1. Marie-Lise Jobin & Sana Siddig & Zsombor Koszegi & Yann Lanoiselée & Vladimir Khayenko & Titiwat Sungkaworn & Christian Werner & Kerstin Seier & Christin Misigaiski & Giovanna Mantovani & Markus Sauer, 2023. "Filamin A organizes γ‑aminobutyric acid type B receptors at the plasma membrane," Nature Communications, Nature, vol. 14(1), pages 1-14, December.

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