Astrocyte-mediated short-term synaptic depression in the rat hippocampal CA1 area: two modes of decreasing release probability

• Published in: BMC neuroscience Vol. 12; no. 1; p. 87
• Main Authors: Andersson, My S, Hanse, Eric
• Format: Journal Article
• Language: English
• Published: England BioMed Central Ltd 24-08-2011; BioMed Central; BMC
• Subjects: Animals; Astrocytes; Astrocytes - physiology; Cells, Cultured; Computer Simulation; Cortical Spreading Depression - physiology; Depression, Mental; Diagnosis; Experiments; Hippocampus (Brain); Hippocampus - physiology; Independent sample; Models, Neurological; Models, Statistical; Neurosciences; Neurovetenskaper; Physiological aspects; Rats; Rats, Wistar; Risk factors; Synaptic Transmission - physiology; Sweden
• ISSN: 1471-2202; 1471-2202
• DOI: 10.1186/1471-2202-12-87

Synaptic burst activation feeds back as a short-term depression of release probability at hippocampal CA3-CA1 synapses. This short-term synaptic plasticity requires functional astrocytes and it affects both the recently active (< 1 s) synapses (post-burst depression) as well as inactive neighboring synapses (transient heterosynaptic depression). The aim of this study was to investigate and compare the components contributing to the depression of release probability in these two different scenarios.
When tested using paired-pulses, following a period of inactivity, the transient heterosynaptic depression was expressed as a reduction in the response to only the first pulse, whereas the response to the second pulse was unaffected. This selective depression of only the first response in a high-frequency burst was shared by the homosynaptic post-burst depression, but it was partially counteracted by augmentation at these recently active synapses. In addition, the expression of the homosynaptic post-burst depression included an astrocyte-mediated reduction of the pool of release-ready primed vesicles.
Our results suggest that activated astrocytes depress the release probability via two different mechanisms; by depression of vesicular release probability only at inactive synapses and by imposing a delay in the recovery of the primed pool of vesicles following depletion. These mechanisms restrict the expression of the astrocyte-mediated depression to temporal windows that are typical for synaptic burst activity.