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Chemical Compound Review

Clorgilin     N-[3-(2,4- dichlorophenoxy)propyl]-N- methyl...

Synonyms: CLORGYLINE, Clorgilina, Clorgiline, Chlorgyline, Clorgilinum, ...
 
 
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Disease relevance of Clorgiline

 

Psychiatry related information on Clorgiline

 

High impact information on Clorgiline

 

Chemical compound and disease context of Clorgiline

 

Biological context of Clorgiline

 

Anatomical context of Clorgiline

  • Following the infusion of clorgyline, the administration of serotonin produced significant decreases in glucose utilisation in cortical areas of between 12 and 33% and in the caudate nucleus of 16% [23].
  • In order to examine the relationship between thyroid status, the circadian system, and antidepressant drug response, the antidepressant drug clorgyline, a monoamine oxidase inhibitor (MAOI), was administered chronically to sham-operated or thyroparathyroidectomized rats [24].
  • In vivo inhibition of type A by clorgyline, and type B by (--)deprenyl, however, tended to decrease the specific activity of both types of MAO to a smaller extent in the female than in the male hypothalamus [25].
  • The binding of N-methyl(R)salsolinol to mitochondria was inhibited by clorgyline, a MOA-A inhibitor, but not by (-)deprenyl, an MAO-B inhibitor [26].
  • The numerical density of dense core vesicles in pinealocyte perikarya increased after treatment with clorgyline [27].
 

Associations of Clorgiline with other chemical compounds

  • However, the neurotoxicity of these two analogs can be prevented by pretreatment with a combination of deprenyl and the selective MAO-A inhibitor clorgyline at doses that are sufficient to almost completely inhibit both MAO-B and MAO-A activities [28].
  • Clorgyline, an inhibitor of monoamine oxidase type A, blocked the formation of oxidized glutathione [29].
  • Essentially all MAO activity in the noradrenergic cultures was inhibited by preincubation with 10(-8)-10(-9) M clorgyline, which indicated that this activity was primarily MAO-A [30].
  • Responses to intravenous clonidine, a possible central noradrenergic probe, were examined in patients with depression before and after treatment with clorgiline, a selective monoamine oxidase type A inhibitor [31].
  • To address these issues, hypothalamic temperature (Thy) was monitored telemetrically in hamsters treated with three antidepressant drugs: the monoamine oxidase inhibitor (MAOI), clorgyline; the 5HT reuptake inhibitor, fluoxetine; and the alkali metal, lithium [32].
 

Gene context of Clorgiline

 

Analytical, diagnostic and therapeutic context of Clorgiline

  • The regional distributions of monoamine oxidase (MAO) types A and B have been identified in human brain in vivo with intravenously injected 11C-labeled suicide enzyme inactivators, clorgyline and L-deprenyl, and positron emission tomography [37].
  • Values similar to this were obtained by clorgyline titration, and both methods gave values similar to those found with a [3H]harmaline binding assay [38].
  • Short term clinical trials have shown that clomipramine is generally more effective than amitriptyline, imipramine, desipramine, nortriptyline or clorgiline in reducing obsessive compulsive symptoms [39].
  • Acute and chronic effects of desipramine and clorgyline on alpha(2)-adrenoceptors regulating noradrenergic transmission in the rat brain: a dual-probe microdialysis study [40].
  • From these, the dose that increased BP by 30 mmHg (ED(30)) was computed for each rabbit before and after oral administration of clorgyline, 1 mg/kg for one week, tranylcypromine 10 mg/kg, once, moclobemide, 20 mg/kg 3 times and TV-3326, 26 mg/kg for 2 weeks [41].

References

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