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Homeostatic Presynaptic Plasticity Is Specifically Regulated by P/Q-type Ca(2+) Channels at Mammalian Hippocampal Synapses
Voltage-dependent Ca(2+) channels (VGCC) represent the principal source of Ca(2+) ions driving evoked neurotransmitter release at presynaptic boutons. In mammals, presynaptic Ca(2+) influx is mediated mainly via P/Q-type and N-type VGCC, which differ in their properties. Changes in their relative co...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Cell Press
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5643522/ https://www.ncbi.nlm.nih.gov/pubmed/29020622 http://dx.doi.org/10.1016/j.celrep.2017.09.061 |
Sumario: | Voltage-dependent Ca(2+) channels (VGCC) represent the principal source of Ca(2+) ions driving evoked neurotransmitter release at presynaptic boutons. In mammals, presynaptic Ca(2+) 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 Ca(2+) 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. |
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