An astrocytic AMPAR-dependent parity signal preserves synaptic strength
Elazar, N.; Ravenel, J. R.; Kim, J.; Vaidyanathan, T.; Wirfel-Farenchak, O.; Uryu, K.; Lim, S. S. X.; Roach, J. R.; Zhang, W.; Cao, X.; van Praag, M. E.; Yan, H.; Yu, G.; Tadross, M. R.; Eroglu, C.
Show abstract
Astrocytic processes closely associate with excitatory synapses and express AMPARs, positioning them to sense the same glutamate signals as neurons. Whether a mismatch between neuronal and astrocytic glutamate sensing affects synaptic physiology is unknown. Using AstroHTP, an extension of Drug Acutely Restricted by Tethering (DART) for cell-type-specific pharmacology, we found that acute astrocytic AMPAR inhibition spared neuronal AMPARs and basal transmission yet converted ongoing glutamatergic activity into a remarkably potent form of long-term depression (LTD) in mouse striatal projection neurons (SPNs). Unlike canonical presynaptic LTD, this form of LTD manifests postsynaptically, requires non-ionotropic NMDA receptor signaling, and arises when glutamate transmission occurs without a matching astrocytic signal. Astrocytic glutamate sensing through AMPARs, therefore, acts as a parity signal that verifies transmission and stabilizes active synapses.
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