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. 2019 Apr 9;11:10. doi: 10.3389/fnsyn.2019.00010

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Copyright © 2019 Valtcheva and Venance.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Effects of EAATs modulation on long-term plasticity. (A,B) Effects of EAATs regulation on rate-based plasticity. (A) Downregulation of EAATs by pharmacological inhibition or genetic knock-out (closed circles) results in a lower threshold for LTD induction and a higher threshold for LTP induction using rate-based plasticity paradigms compared to control conditions (open circles). Pharmacological inhibition of EAATs: (1) increases LTD magnitude (Brasnjo and Otis, 2001); (2) promotes LTD (Massey et al., 2004; Wong et al., 2007); (3) prevents LTP induction (Wang et al., 2006). Genetic knock-out of EAATs; and (4) decreases LTP amplitude (Katagiri et al., 2001; Scimemi et al., 2009). (B) Upregulation of EAATs by chronic ceftriaxone treatment (closed circles) prevents the expression of LFS-induced LTD and decreases the amplitude of HFS-induced LTP compared to control conditions (open circles; Omrani et al., 2009). (C,D) Effects of EAATs regulation on spike-timing-based plasticity. (C) Downregulation of EAAT2 by pharmacological inhibition with DHK results in a broadening of the permissive window (Δt_STDP) for plasticity expression (Valtcheva and Venance, 2016). (D) Upregulation of EAATs by chronic ceftriaxone treatment prevents the expression of STDP (Valtcheva and Venance, 2016).