Journal
JOURNAL OF NEUROSCIENCE
Volume 39, Issue 21, Pages 4051-4065Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.2601-18.2019
Keywords
homeostasis; neuromuscular junction; neurotransmission; plasticity; synapse; synaptic growth
Categories
Funding
- National Institutes of Health [NS091546]
- University of Southern California Undergraduate Research Awards
- University of Southern California Provost Graduate Research Fellowships
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Synapses grow, prune, and remodel throughout development, experience, and disease. This structural plasticity can destabilize information transfer in the nervous system. However, neural activity remains stable throughout life, implying that adaptive countermeasures exist that maintain neurotransmission within proper physiological ranges. Aberrant synaptic structure and function have been associated with a variety of neural diseases, including Fragile X syndrome, autism, and intellectual disability. We have screened 300 mutants in Drosophila larvae of both sexes for defects in synaptic growth at the neuromuscular junction, identifying 12 mutants with severe reductions or enhancements in synaptic growth. Remarkably, electrophysiological recordings revealed that synaptic strength was unchanged in all but one of these mutants compared with WT. We used a combination of genetic, anatomical, and electrophysiological analyses to illuminate three mechanisms that stabilize synaptic strength despite major disparities in synaptic growth. These include compensatory changes in (1) postsynaptic neurotransmitter receptor abundance, (2) presynaptic morphology, and (3) active zone structure. Together, this characterization identifies new mutants with defects in synaptic growth and the adaptive strategies used by synapses to homeostatically stabilize neurotransmission in response.
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