Peptide-induced modulation of synaptic transmission and escape response in Drosophila requires two G-protein-coupled receptors

Document Type

Article

Publication Title

Journal of Neuroscience

Publication Date

11-3-2010

Volume

30

Issue

44

First Page

14724

Last Page

14734

DOI

10.1523/JNEUROSCI.3612-10.2010

ISSN

02706474

Abstract

Neuropeptides are found in both mammals and invertebrates and can modulate neural function through activation of G-protein-coupled receptors (GPCRS). The precise mechanisms by which many of these GPCRs modulate specific signaling cascades to regulate neural function are not well defined. We used Drosophila melanogaster as a model to examine both the cellular and behavioral effects of DPKQDFMRFamide, the most abundant peptide encoded by the dFMRF gene. We show that DPKQDFMRFamide enhanced synaptic transmission through activation of two G-protein-coupled receptors, Fmrf Receptor (FR) and Dromyosupressin Receptor-2 (DmsR-2). The peptide increased both the presynaptic Ca2+ response and the quantal content of released transmitter. Peptide-induced modulation of synaptic function could be abrogated by depleting intracellular Ca2+ stores or by interfering with Ca2+ release from the endoplasmic reticulum through disruption of either the ryanodine receptor or the inositol 1,4,5-trisphosphate receptor. The peptide also altered behavior. Exogenous DPKQDFMRFamide enhanced fictive locomotion; this required both the FR and DmsR-2. Likewise, both receptors were required for an escape response to intense light exposure. Thus, coincident detection of a peptide by two GPCRs modulates synaptic function through effects of Ca2+-induced Ca2+ release, and we hypothesize that these mechanisms are involved in behavioral responses to environmental stress. Copyright © 2010 the authors.

E-ISSN

15292401

PubMed ID

21048131

Link to Full Text

Share

COinS