1 rment of aerobic metabolism caused by 1.5 mM amobarbital.

2 >10-fold less potent than its formula isomer amobarbital [5-ethyl-5'-(3-methylbutyl) barbituric acid]

3 ional naming activation with an intracarotid amobarbital (Amytal) injection procedure (IAP) for langu

4 P), [(3)H]ethidium, [(3)H]tetracaine, [(14)C]amobarbital, and 3-(trifluoromethyl)-3-(m-[(125)I]iodoph

5       The barbiturates tested, secobarbital, amobarbital, and thiamylal, each potentiated NMDA-induce

6  the same derivatives inhibit neither [(14)C]amobarbital binding nor [(125)I]TID photoincorporation,

7 butyl) barbituric acid] in inhibiting [(14)C]amobarbital binding.

8                                       [(14)C]Amobarbital binds to one high-affinity (K(d) = 3.7 micro

9  The cell-impermeant barbiturate N-glucoside amobarbital did not influence mitochondrial potential or

10 guage lateralization testing by intracarotid amobarbital injection showed no evidence of independent

11 ome a viable alternative to the intracarotid amobarbital procedure (IAP), the current gold standard f

12 psies against the results of an intracarotid amobarbital procedure (IAP).

13 efore and during left and right intracarotid amobarbital procedure (IAP).

14   Functional MRI (fMRI) and the intracarotid amobarbital test (IAT) are generally congruent, but fMRI

15  language representation by the intracarotid amobarbital test.

16                                 Intracarotid amobarbital testing (IAT) is currently the most widely u

17 ory profiles were obtained from intracarotid amobarbital testing and non-invasive verbal memory asses

18 y with memory lateralization by intracarotid amobarbital testing.

19  declarative memory capacities (intracarotid amobarbital testing: P < 0.001; verbal memory: P < 0.05)