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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...

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Detalles Bibliográficos
Autores principales: Jeans, Alexander F., van Heusden, Fran C., Al-Mubarak, Bashayer, Padamsey, Zahid, Emptage, Nigel J.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Cell Press 2017
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
Descripción
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.