Main Menu (Mobile)- Block

Main Menu - Block

Axonal Endoplasmic Reticulum Ca(2+) Content Controls Release Probability in CNS Nerve Terminals.

Our Research / Publications
janelia7_blocks-janelia7_biblio_header | block
Neuron. 2017 Jan 30;93(4):867-81. doi: 10.1016/j.neuron.2017.01.010
View Article on
Axonal Endoplasmic Reticulum Ca(2+) Content Controls Release Probability in CNS Nerve Terminals. Schreiter LabGENIE
de Juan-Sanz J, Holt GT, Schreiter ER, de Juan F, Kim DS, Ryan TA
janelia7_blocks-janelia7_biblio_abstract | block

Abstract

Although the endoplasmic reticulum (ER) extends throughout axons and axonal ER dysfunction is implicated in numerous neurological diseases, its role at nerve terminals is poorly understood. We developed novel genetically encoded ER-targeted low-affinity Ca(2+) indicators optimized for examining axonal ER Ca(2+). Our experiments revealed that presynaptic function is tightly controlled by ER Ca(2+) content. We found that neuronal activity drives net Ca(2+) uptake into presynaptic ER although this activity does not contribute significantly to shaping cytosolic Ca(2+) except during prolonged repetitive firing. In contrast, we found that axonal ER acts as an actuator of plasma membrane (PM) function: [Ca(2+)]ER controls STIM1 activation in presynaptic terminals, which results in the local modulation of presynaptic function, impacting activity-driven Ca(2+) entry and release probability. These experiments reveal a critical role of presynaptic ER in the control of neurotransmitter release and will help frame future investigations into the molecular basis of ER-driven neuronal disease states.

PMID: 28162809 [PubMed - indexed for MEDLINE]

node:body | entity_field
janelia7_blocks-janelia7_biblio_authors | block

Janelia Authors

Eric Schreiter
janelia7_blocks-janelia7_biblio_tools | block