Distinct molecular pathways govern presynaptic homeostatic plasticity
Cell Reports. 2021-12-01; 37(11): 110105
DOI: 10.1016/j.celrep.2021.110105
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1. Cell Rep. 2021 Dec 14;37(11):110105. doi: 10.1016/j.celrep.2021.110105.
Distinct molecular pathways govern presynaptic homeostatic plasticity.
Nair AG(1), Muttathukunnel P(2), Müller M(3).
Author information:
(1)Department of Molecular Life Sciences, University of Zurich,
Winterthurerstrasse 190, 8057 Zurich, Switzerland; Department of Neuroscience,
Karolinska Institute, 17177 Stockholm, Sweden.
(2)Department of Molecular Life Sciences, University of Zurich,
Winterthurerstrasse 190, 8057 Zurich, Switzerland; Neuroscience Center Zurich,
University of Zurich/ETH Zurich, 8057 Zurich, Switzerland.
(3)Department of Molecular Life Sciences, University of Zurich,
Winterthurerstrasse 190, 8057 Zurich, Switzerland; Neuroscience Center Zurich,
University of Zurich/ETH Zurich, 8057 Zurich, Switzerland. Electronic address:
.
Presynaptic homeostatic plasticity (PHP) stabilizes synaptic transmission by
counteracting impaired neurotransmitter receptor function through
neurotransmitter release potentiation. PHP is thought to be triggered by
impaired receptor function and to involve a stereotypic signaling pathway.
However, here we demonstrate that different receptor perturbations that
similarly reduce synaptic transmission result in different responses at the
Drosophila neuromuscular junction. While receptor inhibition by the glutamate
receptor (GluR) antagonist γ-D-glutamylglycine (γDGG) is not compensated by PHP,
the GluR inhibitors Philanthotoxin-433 (PhTx) and Gyki-53655 (Gyki) induce
compensatory PHP. Intriguingly, PHP triggered by PhTx and Gyki involve separable
signaling pathways, including inhibition of distinct GluR subtypes, differential
modulation of the active-zone scaffold Bruchpilot, and short-term plasticity.
Moreover, while PHP upon Gyki treatment does not require genes promoting
PhTx-induced PHP, it involves presynaptic protein kinase D. Thus, synapses not
only respond differentially to similar activity impairments, but achieve
homeostatic compensation via distinct mechanisms, highlighting the diversity of
homeostatic signaling.
Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.
DOI: 10.1016/j.celrep.2021.110105
PMCID: PMC8692748
PMID: 34910905 [Indexed for MEDLINE]
Conflict of interest statement: Declaration of interests The authors declare no
competing interests.