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Drosophila Larval NMJ Dissection
Published on: February 4, 2009
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Parvalbumin expression affects synaptic development and physiology at the Drosophila larval NMJ
Tao He1, Michael N Nitabach2, Gregory A Lnenicka3
1a Division of Pulmonary and Critical Care Medicine , David Geffen School of Medicine at UCLA , Los Angeles , CA , USA.
Journal of Neurogenetics
|September 4, 2018
Summary
Buffering presynaptic calcium (Ca2+) with parvalbumin (PV) in Drosophila neurons reduced Ca2+ transients and synaptic facilitation. This led to increased transmitter release and smaller motor terminals, suggesting Ca2+ influences synaptic growth.
Area of Science:
- Neuroscience
- Cell Biology
- Synaptic Physiology
Background:
- Presynaptic calcium (Ca2+) is crucial for synaptic development and function.
- Parvalbumin (PV) is a calcium-binding protein that can buffer intracellular Ca2+.
- Drosophila neurons normally do not express PV, making them a suitable model to study PV's effects.
Purpose of the Study:
- To investigate the role of presynaptic Ca2+ buffering by expressing PV in Drosophila neurons.
- To determine the impact of PV on Ca2+ dynamics, synaptic transmission, and motor terminal structure.
- To explore the relationship between presynaptic Ca2+ levels and synaptic growth.
Main Methods:
- Expressing parvalbumin (PV) in identified Drosophila Ib motor neuron terminals innervating muscle fiber 5.
- Measuring intracellular Ca2+ transients using the fluorescent indicator OGB-1 following single action potentials (APs) and AP trains.
- Performing electrophysiological recordings from muscle fiber 5 to assess synaptic facilitation and transmitter release.
- Utilizing confocal microscopy to analyze the structural changes in motor terminals.
Main Results:
- PV expression reduced the amplitude and decay time constant of Ca2+ transients evoked by single APs.
- For AP trains, PV decreased the rate of rise and decay of intracellular Ca2+ ([Ca2+]i) without affecting the plateau level.
- Paired-pulse facilitation and synaptic enhancement during AP trains were reduced in PV-expressing terminals.
- Transmitter release for single APs increased, potentially as a homeostatic response.
- PV expression led to smaller motor terminals with fewer synaptic boutons and active zones.
Conclusions:
- Buffering presynaptic Ca2+ with PV alters Ca2+ dynamics and reduces synaptic facilitation.
- Reduced Ca2+ transients and facilitation may trigger a homeostatic increase in transmitter release.
- Presynaptic Ca2+ levels appear to play a role in regulating motor terminal growth, with reduced Ca2+ leading to smaller terminals.
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