Bidirectional regulation by "star forces": Ionotropic astrocyte's optical stimulation suppresses synaptic plasticity, metabotropic one strikes back.

Hippocampus 2023

Maltsev A, Roshchin M, Bezprozvanny I

Abstract

  1. Hippocampus. 2023 Jan;33(1):18-36. doi: 10.1002/hipo.23486. Epub 2022 Dec 9.

Bidirectional regulation by “star forces”: Ionotropic astrocyte’s optical stimulation suppresses synaptic plasticity, metabotropic one strikes back.

Maltsev A(1), Roshchin M(1), Bezprozvanny I(2)(3), Smirnov I(1), Vlasova O(2), Balaban P(1), Borodinova A(1).

Author information: (1)Laboratory of Cellular Neurobiology of Learning, Institute of Higher Nervous Activity and Neurophysiology, Russian Academy of Sciences, Moscow, Russia. (2)Laboratory of Molecular Neurodegeneration, Peter the Great St. Petersburg Polytechnic University, St. Petersburg, Russia. (3)Department of Physiology, University of Texas Southwestern Medical Center at Dallas, Dallas, Texas, USA.

The role of astrocytes in modulating synaptic plasticity is an important question that until recently was not addressed due to limitations of previously existing technology. In the present study, we took an advantage of optogenetics to specifically activate astrocytes in hippocampal slices in order to study effects on synaptic function. Using the AAV-based delivery strategy, we expressed the ionotropic channelrhodopsin-2 (ChR2) or the metabotropic Gq-coupled Opto-a1AR opsins specifically in hippocampal astrocytes to compare different modalities of astrocyte activation. In electrophysiological experiments, we observed a depression of basal field excitatory postsynaptic potentials (fEPSPs) in the CA1 hippocampal layer following light stimulation of astrocytic ChR2. The ChR2-mediated depression increased under simultaneous light and electrical theta-burst stimulation (TBS). Application of the type 2 purinergic receptor antagonist suramin prevented depression of basal synaptic transmission, and switched the ChR2-dependent depression into potentiation. The GABAB receptor antagonist, phaclofen, did not prevent the depression of basal fEPSPs, but switched the ChR2-dependent depression into potentiation comparable to

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