ライフサイエンスコーパス: clorgyline

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1 h the moiety derived from the MAOA inhibitor clorgyline.

2 tomography and the MAO-A radiotracer [(11)C]clorgyline.

3 re inhibited by the specific MAO-A inhibitor clorgyline.

4 llowing the same dose of the MAO A inhibitor 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 Littermates were injected with either clorgyline (5 mg/kg) or sterile saline five times daily.

10 Clorgyline administration from birth to postnatal day (P

11 Chronic treatment with clorgyline, an irreversible inhibitor of monoamine oxida

12 riatum and substantia nigra was similar with clorgyline and deprenyl even if the ratio MAO A/MAO B wa

13 stration of the monoamine oxidase inhibitors clorgyline and deprenyl resulted in a 42% and 75% reduct

14 s with the MAO A-specific radiotracers (11)C-clorgyline and deuterium-substituted (11)C-clorgyline ((

15 rreversibly inhibited by the MAO A inhibitor clorgyline and exhibit binding stoichiometries of 0.54 (

16 ectivity toward MAO-A isoenzyme, compared to clorgyline and moclobemide, with Ki values on the picomo

17 "more flexible" than that of MAO B and that clorgyline and pargyline inactivation of MAO A and B, re

18 nonsmokers and 16 current smokers with [11C]clorgyline and positron emission tomography (PET).

19 on to three MAO inhibitors, tranylcypromine, clorgyline, and pargyline.

20 with the monoamine oxidase inhibitor (MAOI), clorgyline, and then injected with 8-OH-DPAT or vehicle

21 rescanned to assess the sensitivity of [11C]clorgyline binding to MAO inhibition.

22 ist, can be modified by the MAO(A) inhibitor clorgyline, by a mechanism apparently unrelated to its a

23 rature in response to challenge injection of clorgyline combined with the SSRI paroxetine.

24 euterium-substituted (11)C-clorgyline ((11)C-clorgyline-D2) using the deuterium isotope effect to ass

25 a severe level in rats pretreated with daily clorgyline for 3 and 6 days but not in rats pretreated f

26 rats by once daily pretreatment of the MAOI clorgyline for 3, 6, or 13 days.

27 Animals treated with clorgyline from birth to P6 and killed on P8 or P10 had

28 Quinpirole-sensitized rats pretreated with clorgyline had similar alterations in LCGU, but LCGU was

29 oichiometric amounts of both (-)deprenyl and clorgyline in a mechanism-based reaction, forming flavoc

30 sidues modified by biotin-derivatized NEM in clorgyline-inactivated MAO A and pargyline-inactivated M

31 cked by inhibition of monoamine oxidase with clorgyline indicating that accumulation of DOPAL was res

32 aphy using a radioligand specific for MAO A (clorgyline labeled with carbon 11).

33 deprenyl (MAO B-specific inhibitor) than to clorgyline (MAO A-specific inhibitor).

34 A treatment was preceded by the injection of clorgyline or deprenyl at a concentration (1 mg/kg) whic

35 the monoamine (MAO) inhibitors, l-deprenyl, clorgyline, pargyline, or in vivo nialamide produced 30-

36 n quinpirole-sensitized rats with or without clorgyline pretreatment were assessed based on LCGU usin

37 ified behavioral response to quinpirole with clorgyline pretreatment.

38 nzymes, but inactivation is much faster with clorgyline than deprenyl, suggesting a closer resemblanc

39 and, similar to MAO A, was more sensitive to clorgyline than to deprenyl.

40 step for the irreversible binding of labeled clorgyline to MAO A.

41 colocalized with the islets of Langerhans in clorgyline-treated animals.

42 gher retention of the radiopharmaceutical in clorgyline-treated animals.

43 For example, clorgyline-treated Cplx2-/- mice spent significantly mor

44 yer IV cellular aggregates demonstrated that clorgyline treatment from P0 to P6 produced a complete a

45 These results indicate that clorgyline treatment produces a transient disruption of

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