Homeostatic Presynaptic Plasticity Is Specifically Regulated by P/Q-type Ca2+ Channels at Mammalian Hippocampal Synapses

Alexander F Jeans, Fran C van Heusden, Bashayer Al-Mubarak, Zahid Padamsey, Nigel J Emptage

Research output: Contribution to journalArticlepeer-review

Abstract / Description of output

Voltage-dependent Ca2+ channels (VGCC) represent the principal source of Ca2+ ions driving evoked neurotransmitter release at presynaptic boutons. In mammals, presynaptic Ca2+ influx is mediated mainly via P/Q-type and N-type VGCC, which differ in their properties. Changes in their relative contributions tune neurotransmission both during development and in Hebbian plasticity. However, whether this represents a functional motif also present in other forms of activity-dependent regulation is unknown. Here, we study the role of VGCC in homeostatic plasticity (HSP) in mammalian hippocampal neurons using optical techniques. We find that changes in evoked Ca2+ currents specifically through P/Q-type, but not N-type, VGCC mediate bidirectional homeostatic regulation of both neurotransmitter release efficacy and the size of the major synaptic vesicle pools. Selective dependence of HSP on P/Q-type VGCC in mammalian terminals has important implications for phenotypes associated with P/Q-type channelopathies, including migraine and epilepsy.

Original languageEnglish
Pages (from-to)341-350
Number of pages10
JournalCell Reports
Volume21
Issue number2
DOIs
Publication statusPublished - 10 Oct 2017

Keywords / Materials (for Non-textual outputs)

  • Animals
  • Calcium Channels, L-Type/metabolism
  • Calcium Channels, P-Type/metabolism
  • Cells, Cultured
  • Hippocampus/cytology
  • Homeostasis
  • Mice
  • Neuronal Plasticity
  • Neurons/metabolism
  • Presynaptic Terminals/metabolism
  • Rats
  • Synaptic Vesicles/metabolism

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