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Phosphorylation-dependent low-frequency depression at phasic synapses of a crayfish motoneuron
Lorelei B Silverman-Gavrila1, Peter M R Orth, Milton P Charlton
1Department of Physiology, University of Toronto, Toronto, Ontario, Canada M5S 1A8.
Summary
Low-frequency depression (LFD) at phasic synapses involves phosphorylation. Protein kinases and phosphatases regulate this presynaptic event, impacting neurotransmitter release and synaptic plasticity.
Area of Science:
- Neuroscience
- Cell Biology
- Synaptic Physiology
Background:
- Phascial synapses exhibit high neurotransmitter release probability.
- Low-frequency depression (LFD) is a presynaptic event affecting transmitter release.
- Understanding LFD mechanisms is crucial for synaptic plasticity research.
Purpose of the Study:
- To investigate the role of phosphorylation in low-frequency depression (LFD) at crayfish phasic synapses.
- To elucidate the involvement of protein kinases and phosphatases in regulating presynaptic function during LFD.
Main Methods:
- Intracellular recordings from crayfish leg extensor muscle.
- Stimulation protocols to induce LFD at 0.2 Hz.
- Pharmacological manipulation of protein kinases and phosphatases (1A/2A, calcineurin).
- Immunostaining for calcineurin-like immunoreactivity.
Main Results:
- LFD occurred over time with time constants of 4 and 105 min.
- Blockade of protein kinases accelerated LFD; kinase stimulation reduced depression.
- Blockade of protein phosphatases reversed LFD; calcineurin inhibition abolished LFD and induced facilitation.
- Recovery from LFD was blocked by kinase inhibition.
Conclusions:
- Phosphorylation-dependent mechanisms are critical for LFD at phasic synapses.
- The balance between protein kinases and phosphatases controls presynaptic exocytosis.
- Synaptic plasticity is modulated by shifts in the phosphorylation state of key substrates.