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. Author manuscript; available in PMC: 2014 Jan 30.
Published in final edited form as: Neurobiol Dis. 2010 Mar 19;38(3):434–445. doi: 10.1016/j.nbd.2010.03.003

Fig. 6.

Fig. 6

A2AR antagonism rescues striatal synaptic plasticity impairments in hMT mice. Preincubation of the slices with the A2AR antagonist SCH 58261 (50 nM, 20 min) restores LTD in hMT mice, without modifying the time-course in NT and hWT mice (a). Below, sample EPSPs recorded before (pre) and after (post) HFS. (b) In the absence of external magnesium, HFS (arrow) induces a robust LTP in the three genotypes. Once obtained a stable LTP, a low-frequency stimulation protocol (LFS) is able to revert synaptic potentiation to resting level, both in NT and hWT mice, but not in hMT slices. Below, representative traces showing EPSPs before and after HFS, as well as after LFS in hWT and hMT mice. (c) Pretreatment of the tissue with SCH 58261 rescues synaptic depotentiation. Sample EPSPs recorded before (left), after HFS (middle trace), and after the LFS protocol (right). In hMT mice, SCH 58261 restores a physiological synaptic depotentiation.