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 language | English |
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Pages (from-to) | 341-350 |
Number of pages | 10 |
Journal | Cell Reports |
Volume | 21 |
Issue number | 2 |
DOIs | |
Publication status | Published - 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