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Presynaptic HCN channels regulate vesicular glutamate transport
Hai Huang1, Laurence O Trussell2
1Oregon Hearing Research Center & Vollum Institute, Oregon Health and Science University, 3181 SW Sam Jackson Park Road, L335A, Portland, OR 97239, USA; Department of Cell and Molecular Biology, Tulane University, 2000 Percival Stern Hall, 6400 Freret Street, New Orleans, LA 70118, USA.
Neuron
|September 30, 2014
Summary
Presynaptic sodium (Na+) concentration regulates neurotransmitter uptake into vesicles, controlling synaptic strength. This process involves hyperpolarization-activated cyclic nucleotide-gated (HCN) channels and a Na+-dependent mechanism.
Area of Science:
- Neuroscience
- Cellular Biology
- Synaptic Transmission
Background:
- Vesicular neurotransmitter storage is crucial for synaptic transmission strength.
- Regulation of vesicular neurotransmitter uptake remains poorly understood.
Purpose of the Study:
- To investigate the regulation of vesicular neurotransmitter uptake.
- To identify mechanisms controlling synaptic strength at the presynaptic terminal.
Main Methods:
- Electrophysiological recordings from the calyx of Held, a giant glutamatergic synapse.
- Manipulation of presynaptic sodium (Na+) concentration.
- Analysis of vesicular glutamate uptake and postsynaptic quantal size.
Main Results:
- Presynaptic Na+ concentration directly regulates vesicular glutamate uptake.
- A Na+(K+)/H+ exchanger is involved in vesicular uptake.
- Na+ flux through hyperpolarization-activated cyclic nucleotide-gated (HCN) channels enhances presynaptic Na+ concentration, controlling quantal size.
Conclusions:
- Plasma membrane ion channels, specifically HCN channels, control synaptic strength.
- Synaptic strength is modulated by a Na+-dependent mechanism regulating vesicular neurotransmitter uptake.
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