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Published on: February 26, 2018
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Synapse-specific catecholaminergic modulation of neuronal glutamate release.
Dariya Bakshinska1,2, William YuChen Liu2, Ryan Schultz1
1Helen Wills Neuroscience Institute, University of California Berkeley, Berkeley, CA 94720.
Summary
Octopamine enhances glutamate release in hungry Drosophila larvae by acting on specific motor neurons. This fine-tuning of synaptic potentiation regulates complex locomotor behaviors.
Area of Science:
- Neuroscience
- Molecular Biology
- Animal Behavior
Background:
- Octopamine and norepinephrine are key neuromodulators regulating neural circuits in invertebrates and vertebrates, respectively.
- Hunger state in Drosophila larvae triggers changes in motor neuron activity, influencing locomotion.
Purpose of the Study:
- To investigate the precise mechanism by which octopamine modulates glutamate release in Drosophila motor neurons.
- To elucidate the molecular players involved in octopamine's potentiation of synaptic transmission.
Main Methods:
- Simultaneous optical quantal analysis of hundreds of synapses in Drosophila larvae.
- Investigated the role of the Gq-coupled octopamine receptor (OAMB) and Unc13A in synaptic potentiation.
- Differentiated between tonic type Ib and phasic type Is motor neurons.
Main Results:
- Octopamine potentiates glutamate release specifically in tonic type Ib motor neurons, not phasic type Is.
- This potentiation is mediated by the OAMB receptor, diacylglycerol, and Unc13A.
- Synaptic potentiation varied up to 1,000% across synapses, with Unc13A levels dictating release probability and potentiation.
Conclusions:
- A dual molecular mechanism involving OAMB and Unc13A fine-tunes octopaminergic modulation of synaptic transmission.
- Differential potentiation of tonic versus phasic synapses allows for sophisticated regulation of locomotor behavior in response to hunger.
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