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Whole-cell Patch-clamp Recordings from Morphologically- and Neurochemically-identified Hippocampal Interneurons
Published on: September 30, 2014
Dendritic Ca2+ channels characterized by recordings from isolated hippocampal dendritic segments
1Department of Molecular and Cellular Physiology, Beckman Center, Stanford University School of Medicine, California 94305-5426, USA.
Neuron
|April 1, 1997
Summary
Low voltage-activated T-type calcium channels contribute significantly to calcium influx in dendrites. High voltage-activated channels in dendrites are sensitive to neurotransmitter inhibition, revealing new roles in neuronal signaling.
Area of Science:
- Neuroscience
- Cellular Biology
- Electrophysiology
Background:
- Dendritic arbors are crucial for neuronal information processing.
- Geometric complexity of dendrites hinders quantitative analysis of membrane properties.
- Voltage-gated calcium channels are a key source of calcium entry in dendrites.
Purpose of the Study:
- To quantitatively analyze the contribution of different voltage-gated calcium channels to calcium influx in isolated dendritic segments.
- To investigate the susceptibility of dendritic calcium channels to neurotransmitter inhibition.
Main Methods:
- Whole-cell voltage-clamp technique applied to isolated dendritic segments (dendrosomes) from rat hippocampal neurons.
- Characterization of calcium (Ca2+) currents through different types of voltage-gated calcium channels.
Main Results:
- Low voltage-activated T-type calcium channels account for a larger fraction of dendritic Ca2+ influx compared to cell bodies.
- N-type and P/Q-type calcium channels constitute 60%-70% of the high voltage-activated Ca2+ current in dendrosomes.
- Dendritic high voltage-activated Ca2+ channels are susceptible to inhibition by neurotransmitters.
Conclusions:
- Dendritic T-type calcium channels play a significant role in regulating dendritic excitability and calcium signaling.
- Neurotransmitter-mediated inhibition of N-type and P/Q-type calcium channels suggests a novel mechanism for controlling dendritic excitability.
- These findings highlight a new physiological role for G protein-regulated calcium channel modulation in central neurons.

