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Published on: April 23, 2019
Ca(2+)-dependent enhancement of release by subthreshold somatic depolarization
Jason M Christie1, Delia N Chiu, Craig E Jahr
1Vollum Institute, Oregon Health & Science University, Portland, Oregon, USA. jason.christie@maxplanckflorida.org
Subthreshold somatic depolarization in cerebellar neurons strengthens synaptic release via calcium influx into the axon. This calcium-dependent mechanism modulates neuronal communication and presynaptic plasticity.
Area of Science:
- Neuroscience
- Cellular Biology
- Neurophysiology
Background:
- Subthreshold somatic depolarization influences axonal electrical activity and synaptic transmission.
- Intracellular calcium (Ca2+) is a key regulator of neurotransmitter release probability.
- The precise role of Ca2+ in subthreshold depolarization-mediated synaptic modulation remains debated.
Purpose of the Study:
- To investigate the Ca2+ dependence of synaptic release modulation by subthreshold somatic depolarization in cerebellar neurons.
- To elucidate the mechanisms by which somatic depolarization affects axonal Ca2+ dynamics and release probability.
Main Methods:
- Paired recordings from synaptically connected molecular layer interneurons (MLIs) in the rat cerebellum.
- Two-photon microscopy to visualize Ca2+ dynamics at the axon.
- Experimental manipulation of intracellular Ca2+ using exogenous buffering.
Main Results:
- Brief subthreshold somatic depolarization led to Ca2+-mediated strengthening of synaptic release.
- Somatic depolarization induced Ca2+ influx at the axon via voltage-sensitive Ca2+ channels, enhancing spike-evoked Ca2+ entry.
- Reduced axonal Ca2+ transients through buffering eliminated the observed release strengthening.
- Axonal Ca2+ influx also triggered asynchronous transmission, potentially impacting vesicle availability.
Conclusions:
- Activity-dependent presynaptic plasticity in the cerebellum relies on Ca2+ elevations from both sub- and suprathreshold somatic activity.
- Subthreshold somatic depolarization plays a significant role in modulating synaptic transmission through axonal Ca2+ dynamics.
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