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1 tivity and actually potentiated responses to alphaxalone.
2 , etomidate, or pentobarbital or the steroid alphaxalone.
7 perception, and anesthetic steroids such as alphaxalone and allopregnanolone, which have a 5alpha-co
8 BA binding) reduced the currents elicited by alphaxalone and pentobarbital from wild-type GABAA recep
10 ne), 5alpha-pregnane-3alpha-ol-11, 20-dione (alphaxalone), and 5alpha-pregnane-3alpha-ol-20-one (allo
11 a partial block of response pentobarbital or alphaxalone, and bicuculline only partially blocked resp
12 C-20 carbonyl group, that prevents Delta(16)-alphaxalone from interacting strongly with the GABA(A) r
13 were more potent than the anesthetic steroid alphaxalone in their threshold for and duration of loss
14 3-hydroxypregn-16-ene-11,20-dione (Delta(16)-alphaxalone) is explained by the steroid Delta(16) doubl
15 l enhanced less than 0.5-fold; etomidate and alphaxalone modulation was reduced from more than 4- to
16 esence of the C-21 methyl group in Delta(16)-alphaxalone, not the location of the constrained C-20 ca
17 he barbiturate methohexital, and the steroid alphaxalone on wild-type and mutant GABAA receptors expr
18 dicate that the blockers do not compete with alphaxalone or pentobarbital for a single class of sites
19 lesser extent by either chlordiazepoxide or alphaxalone than are the responses of B-type neurons, in
20 16) and Delta(17(20)) analogues of Delta(16)-alphaxalone was prepared to evaluate this hypothesis in
21 ts by propofol, etomidate, pentobarbital, or alphaxalone were at similar or lower drug concentrations
22 se sites did not bind the anesthetic steroid alphaxalone, which enhanced photolabeling, or DS-2, a de
23 alpha,5alpha)-3-hydroxypregnane-11,20-dione (alphaxalone) with regard to time of onset and rate of re
24 usion, a Delta(17(20)) analogue of Delta(16)-alphaxalone without a C-21 methyl group was found to be
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