Noradrenergic function and depression, too much or too little?
Antithetical hypotheses as to CNS noradrenergic function in depressed patients can be constructed from results of pharmacological studies of the effects of antidepressant drugs. The experimental data supporting each of these opposing propositions is briefly reviewed in this paper. Finally, the results of clinical studies of noradrenergic function in depressed patients are noted and discussed in terms of these disparate hypotheses.
D000661:Amphetamine / Q000627:therapeutic use; D001714:Bipolar Disorder / Q000378:metabolism*; D001921:Brain / Q000201:enzymology; D001923:Brain Chemistry; D003891:Desipramine / Q000627:therapeutic use; D004565:Electroconvulsive Therapy; D006801:Humans; D007099:Imipramine / Q000627:therapeutic use; D007488:Iprindole / Q000627:therapeutic use; D008734:Methoxyhydroxyphenylglycol / Q000652:urine; D009638:Norepinephrine / Q000032:analysis / Q000378:metabolism*; D012436:S-Adenosylmethionine / Q000032:analysis; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism
D008734:Methoxyhydroxyphenylglycol; D007488:Iprindole; D012436:S-Adenosylmethionine; D000661:Amphetamine; D014446:Tyrosine 3-Monooxygenase; D007099:Imipramine; D003891:Desipramine; D009638:Norepinephrine