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J Neurosci. 2015 Jan 21;35(3):1038-42. doi: 10.1523/JNEUROSCI.2825-14.2015.

NLP-12 engages different UNC-13 proteins to potentiate tonic and evoked release.

Author information

1
Department of Molecular Biology, Massachusetts General Hospital, Boston, Massachusetts 02114, Department of Neurobiology, Harvard Medical School, Boston, Massachusetts 02115, and.
2
Department of Molecular Biology, Massachusetts General Hospital, Boston, Massachusetts 02114, Department of Neurobiology, Harvard Medical School, Boston, Massachusetts 02115, and Department of Communication Sciences and Disorders, Emerson College, Boston, Massachusetts 02116.
3
Department of Molecular Biology, Massachusetts General Hospital, Boston, Massachusetts 02114, Department of Neurobiology, Harvard Medical School, Boston, Massachusetts 02115, and kaplan@molbio.mgh.harvard.edu.

Abstract

A neuropeptide (NLP-12) and its receptor (CKR-2) potentiate tonic and evoked ACh release at Caenorhabditis elegans neuromuscular junctions. Increased evoked release is mediated by a presynaptic pathway (egl-30 Gαq and egl-8 PLCβ) that produces DAG, and by DAG binding to short and long UNC-13 proteins. Potentiation of tonic ACh release persists in mutants deficient for egl-30 Gαq and egl-8 PLCβ and requires DAG binding to UNC-13L (but not UNC-13S). Thus, NLP-12 adjusts tonic and evoked release by distinct mechanisms.

KEYWORDS:

C. elegans; CCK; Munc13; NLP-12; UNC-13; neuropeptide

PMID:
25609620
PMCID:
PMC4300317
DOI:
10.1523/JNEUROSCI.2825-14.2015
[Indexed for MEDLINE]
Free PMC Article

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