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Altered impulse activity modifies synaptic physiology and mitochondria in crayfish phasic motor neurons
1Department of Physiology, Faculty of Medicine, University of Toronto, Ontario, Canada.
Journal of Neurophysiology
|December 1, 1994
Summary
Activity-induced long-term adaptation (LTA) enhances synaptic stamina in crayfish motor neurons by increasing mitochondrial oxidative competence. This adaptation requires axonal transport, suggesting a crucial link between mitochondrial function and synaptic fatigue resistance.
Area of Science:
- Neuroscience
- Cell Biology
- Physiology
Background:
- Crayfish phasic motor synapses exhibit rapid fatigue during high-frequency stimulation.
- Long-term adaptation (LTA) can reduce synaptic depression and enhance synaptic stamina.
Purpose of the Study:
- To investigate if activity-induced synaptic fatigue-resistance during LTA is dependent on mitochondrial oxidative competence.
- To explore the correlation between mitochondrial function and enhanced synaptic stamina.
Main Methods:
- In vivo conditioning stimulation of crayfish abdominal extensor motor neurons (axon 3).
- Pharmacological inhibition of mitochondrial ATP synthesis using dinitrophenol and sodium azide.
- Confocal microscopy to assess mitochondrial rhodamine-123 (Rh123) fluorescence.
- Axotomy to investigate the role of axonal transport.
Main Results:
- Periodic stimulation induced LTA, reducing synaptic depression and increasing synaptic stamina.
- Inhibition of mitochondrial ATP synthesis exacerbated synaptic depression in conditioned axons.
- Conditioned axons showed significantly higher mitochondrial Rh123 fluorescence, indicating increased oxidative competence.
- Axotomy prevented the induction of both increased synaptic stamina and enhanced mitochondrial fluorescence.
Conclusions:
- Activity-induced LTA enhances synaptic stamina in crayfish motor neurons.
- Increased mitochondrial oxidative competence is correlated with and dependent upon enhanced synaptic stamina.
- Axonal transport is essential for the induction of both synaptic adaptation and mitochondrial changes.