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. Author manuscript; available in PMC: 2014 Aug 7.
Published in final edited form as: Neuron. 2013 Aug 7;79(3):10.1016/j.neuron.2013.06.003. doi: 10.1016/j.neuron.2013.06.003

Figure 6. State Dependence of Lobe 1 Metal Sites.

Figure 6

(A) The half-maximal inhibitory concentration of zinc for the mutant G437H-K439H-D456H (HHH, yellow circles) was 95 ± 30 nM (n = 4).

(B) Voltage-independent inhibition by zinc (Zn2+; 1 μM, red bar) at intermediate glutamate concentration (500 μM, −60 and +60 mV) is shown. The lower dashed line shows the average size of the control responses to 10 mM glutamate in EDTA (green bars). The lower trace shows a mono-exponential fit to trapping relaxation (red circles, τ = 220 ms) and the slow component of a double exponential fit to current in EDTA (green bar) following trapping (green circles, loss of zinc trapping, τ = 550 ms; amplitude 33%).

(C) State dependence of inhibition by 1 μM zinc (n = 3–6 patches per point). Zinc preferentially traps a partially glutamate-bound state (yellow, 500 μM Glu + CTZ).

(D) WT receptors are not trapped by 1 μM zinc in the presence of 500 μM Glu plus CTZ.

(E) Concentration-response curves in 1 μM zinc and 100 μM CTZ for WT GluA2 (blue open circles; EC50 = 140 ± 10 μM), GluA2 HHH before trapping by zinc (green triangles; EC50 = 230 ± 27 μM), and GluA2 HHH following trapping (red squares; EC50 = 424 ± 30 μM). The difference between the apparent affinities for glutamate in the presence and absence of zinc was significant (p<0.01). Plotting the active fraction current after trapping (yellow diamonds) versus glutamate concentration reveals maximal trapping at 368 μM glutamate (n = 3).

(F) Top view of the CA conformation of the LBD tetramer modeled with two interdimer triple-histidine mutants coordinating zinc ions is presented. The right panel shows the boxed region from the left panel on an expanded scale.