1 gue adenylylimidodiphosphate (AMP(PNP)) and 'Mg2(+)-free' ATP produced little change in the Po of the

2 parison of these structures with that of the Mg2+-free complex revealed Mg2+ bound at the same site a

3 ced in switch II, which is disordered in the Mg2+-free complex, but no order is observed in the switc

4 action of Palphabeta from rod membranes by a Mg2+-free hypotonic buffer.

5            Exposure of hippocampal slices to Mg2+ free media (0 Mg) has been shown to trigger full pr

6    In contrast, driving synaptic activity in Mg2+-free media to hyperactivate synaptic NMDA receptors

7               Supplementation of Ca2(+)- and Mg2(+)-free medium with these cations restored the bacte

8 tion of mixed neuronal and glial cultures in Mg2+-free medium resulted in a decline in cellular total

9 TP more potently than ATP, amplified in Ca2+/Mg2+-free medium, and blocked by PPADS or oxidized ATP.

10 n the multiple population spikes recorded in Mg2+-free medium, and, in grease-gap recordings from the

11 n cultured neurons were treated with NMDA in Mg2+-free medium.

12 ual bound ADP was minimized by incubation in Mg2+-free rigor solution containing 15 mM EDTA.

13 d for 30-60 min with extracellular Ca2+- and Mg2+-free solution contracted following readmission of e

14                Addition of EGTA to Ca2+- and Mg2+-free solution greatly potentiates Na+ influx and ve

15 al slices from first postnatal week mice, in Mg2+-free solution with GABA(A) receptor-mediated inhibi

16           When EGTA was present in Ca2+- and Mg2+-free solution, a significant nifedipine-sensitive N

17 he intrinsic voltage dependence of TREK-2 in Mg2+-free solution.

18      Channel activation was also observed in Mg2+-free solutions and blocked by low (0.1-10 microM) c

19 nformation when compared with the wild-type, Mg2+-free structure, but there are localized changes wit