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1 re inhibited by the specific MAO-A inhibitor clorgyline.
2 h the moiety derived from the MAOA inhibitor clorgyline.
3 llowing the same dose of the MAO A inhibitor clorgyline.
4 tomography and the MAO-A radiotracer [(11)C]clorgyline.
5 e or dopamine or the IC(50) for deprenyl and clorgyline.
6 d with the monoamine oxidase (MAO) inhibitor clorgyline.
7 up) were subjected to an injection of either clorgyline (1.0 mg/kg, s.c.) or saline 90 min prior to a
8 C-clorgyline and deuterium-substituted (11)C-clorgyline ((11)C-clorgyline-D2) using the deuterium iso
9 d by the monoamine oxidase (MAO)-A inhibitor clorgyline (43.9% +/- 4.6%; n = 3), indicating off-targe
13 riatum and substantia nigra was similar with clorgyline and deprenyl even if the ratio MAO A/MAO B wa
14 stration of the monoamine oxidase inhibitors clorgyline and deprenyl resulted in a 42% and 75% reduct
15 s with the MAO A-specific radiotracers (11)C-clorgyline and deuterium-substituted (11)C-clorgyline ((
16 rreversibly inhibited by the MAO A inhibitor clorgyline and exhibit binding stoichiometries of 0.54 (
17 ectivity toward MAO-A isoenzyme, compared to clorgyline and moclobemide, with Ki values on the picomo
18 "more flexible" than that of MAO B and that clorgyline and pargyline inactivation of MAO A and B, re
21 with the monoamine oxidase inhibitor (MAOI), clorgyline, and then injected with 8-OH-DPAT or vehicle
23 ist, can be modified by the MAO(A) inhibitor clorgyline, by a mechanism apparently unrelated to its a
24 aling with the antidepressants phenelzine or clorgyline can restore Enz sensitivity to suppress EnzR
26 euterium-substituted (11)C-clorgyline ((11)C-clorgyline-D2) using the deuterium isotope effect to ass
27 a severe level in rats pretreated with daily clorgyline for 3 and 6 days but not in rats pretreated f
30 Quinpirole-sensitized rats pretreated with clorgyline had similar alterations in LCGU, but LCGU was
31 oichiometric amounts of both (-)deprenyl and clorgyline in a mechanism-based reaction, forming flavoc
32 sidues modified by biotin-derivatized NEM in clorgyline-inactivated MAO A and pargyline-inactivated M
33 cked by inhibition of monoamine oxidase with clorgyline indicating that accumulation of DOPAL was res
36 A treatment was preceded by the injection of clorgyline or deprenyl at a concentration (1 mg/kg) whic
37 the monoamine (MAO) inhibitors, l-deprenyl, clorgyline, pargyline, or in vivo nialamide produced 30-
38 n quinpirole-sensitized rats with or without clorgyline pretreatment were assessed based on LCGU usin
40 nzymes, but inactivation is much faster with clorgyline than deprenyl, suggesting a closer resemblanc
47 yer IV cellular aggregates demonstrated that clorgyline treatment from P0 to P6 produced a complete a