Astrocytes Potentiate Transmitter Release at Single Hippocampal Synapses

TLDR

Astrocytes actively modulate neuronal excitability and synaptic function in the brain. The study aims to determine how astrocytes influence synaptic transmission and plasticity at single hippocampal synapses. Astrocytic Ca²⁺‑dependent glutamate release via SNARE proteins activates mGluRs to mediate short‑term plasticity. Astrocytic Ca²⁺ spikes transiently raise transmitter release probability at CA3‑CA1 synapses, and when paired with postsynaptic depolarization, produce persistent, mGluR‑mediated but NMDA‑independent potentiation, underscoring astrocytes’ role in synaptic information storage.

Abstract

Astrocytes play active roles in brain physiology. They respond to neurotransmitters and modulate neuronal excitability and synaptic function. However, the influence of astrocytes on synaptic transmission and plasticity at the single synapse level is unknown. Ca(2+) elevation in astrocytes transiently increased the probability of transmitter release at hippocampal area CA3-CA1 synapses, without affecting the amplitude of synaptic events. This form of short-term plasticity was due to the release of glutamate from astrocytes, a process that depended on Ca(2+) and soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) protein and that activated metabotropic glutamate receptors (mGluRs). The transient potentiation of transmitter release became persistent when the astrocytic signal was temporally coincident with postsynaptic depolarization. This persistent plasticity was mGluR-mediated but N-methyl-d-aspartate receptor-independent. These results indicate that astrocytes are actively involved in the transfer and storage of synaptic information.