Abstract
Many neurons typically fire action potentials in brief, high-frequency bursts with specific consequences for their synaptic output. Here we have examined short-term plasticity engaged during burst activation using electrophysiological recordings in acute rat hippocampal slices. We show that CA3-CA1 glutamate synapses exhibit a prominent depression of presynaptic release probability for approximately 1 s after such a burst. This postburst depression exhibits a distinct cooperativity threshold, is abolished by inhibiting astrocyte metabolism and astrocyte calcium signaling, and is not operational in the developing hippocampus. Our results suggest that astrocytes are actively involved in short-term synaptic depression, shaping synaptic activity during behaviorally relevant neural activity.
Original language | English |
---|---|
Pages (from-to) | 5776-80 |
Number of pages | 5 |
Journal | The Journal of Neuroscience : the official journal of the Society for Neuroscience |
Volume | 30 |
Issue number | 16 |
DOIs | |
Publication status | Published - 2010 Apr 21 |
Externally published | Yes |
Free keywords
- Animals
- Astrocytes
- CA1 Region, Hippocampal
- CA3 Region, Hippocampal
- Glutamic Acid
- Hippocampus
- Long-Term Synaptic Depression
- Neuronal Plasticity
- Probability
- Rats
- Rats, Wistar
- Receptors, Glutamate
- Synapses
- Comparative Study
- Journal Article
- Research Support, Non-U.S. Gov't