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Evaluation of Synaptic Multiplicity Using Whole-cell Patch-clamp Electrophysiology
Published on: April 23, 2019
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Action potential broadening in a presynaptic channelopathy
Rahima Begum1, Yamina Bakiri1, Kirill E Volynski1
1UCL Institute of Neurology, University College London, Queen Square, London WC1N 3BG, UK.
Nature Communications
|July 7, 2016
Summary
Episodic ataxia type 1, caused by Kv1.1 channel mutations, broadens presynaptic spikes in cerebellar basket cells. This dysfunction increases calcium influx and GABA release, with no evidence of developmental compensation.
Area of Science:
- Neuroscience
- Channelopathies
- Synaptic Plasticity
Background:
- Paroxysmal neurological channelopathies often show unaffected brain development and function, potentially due to homeostatic plasticity.
- Episodic ataxia type 1 results from Kv1.1 potassium channel mutations, crucial for cerebellar basket cell terminals.
Purpose of the Study:
- To investigate presynaptic action potential characteristics in cerebellar basket cells with Kv1.1 dysfunction.
- To determine if developmental plasticity compensates for inherited Kv1.1 channel defects.
Main Methods:
- Visually targeted patch-clamp recordings from mouse cerebellar basket cell terminals.
- Analysis of presynaptic spike broadening and its effects on calcium influx and neurotransmitter release.
Main Results:
- Presynaptic spikes in Kv1.1 mutant mice showed broadening, similar to pharmacological Kv1.1 blockade.
- Spike broadening increased Ca(2+) influx and GABA release, reducing Purkinje cell firing.
- No evidence of developmental compensation for Kv1.1 dysfunction was observed.
Conclusions:
- Inherited Kv1.1 dysfunction directly impacts presynaptic function in cerebellar basket cells.
- Spike broadening and altered neurotransmission contribute to episodic ataxia type 1 pathophysiology.
- Developmental plasticity does not compensate for Kv1.1 channel defects in this model.
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