Platelet imipramine binding in endogenous depressed patients and controls: relationship to platelet MAO and 5HT uptake during successful imipramine treatment.
Platelet imipramine binding was measured in 25 unmedicated depressed patients and 25 age- and sex-matched healthy controls. In the patients, the measurement was repeated after 3 weeks and 2 months of imipramine treatment leading to clinical recovery. No significant differences in imipramine binding were found between controls and unmedicated patients. In the latter, imipramine administration produced a progressive change in the binding characteristics, increasing the apparent Kd and decreasing the number of binding sites (Bmax). The results suggest that platelet imipramine binding is not altered in depression and that changes in this parameter are the consequence of the presence of imipramine in the blood stream. However, such changes accompany changes in other biological parameters, such as platelet monoamine oxidase and serotonin uptake, seen in the same patients throughout imipramine treatment, suggesting that the drug acts on a wide range of normal or altered serotonin-related cellular mechanisms while it accelerates the clinical recovery from depression.
Quintana
J
J
Department of Neurology, School of Medicine, University of California, Los Angeles.
D000284:Administration, Oral; D000328:Adult; D001792:Blood Platelets / Q000187:drug effects* / Q000201:enzymology; D002352:Carrier Proteins; D003866:Depressive Disorder / Q000188:drug therapy* / Q000201:enzymology; D005260:Female; D006801:Humans; D007099:Imipramine / Q000493:pharmacokinetics / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D008995:Monoamine Oxidase / Q000097:blood*; D011955:Receptors, Drug; D017981:Receptors, Neurotransmitter / Q000187:drug effects*; D012701:Serotonin / Q000097:blood*
D002352:Carrier Proteins; D011955:Receptors, Drug; D017981:Receptors, Neurotransmitter; C027775:imipramine receptor; D012701:Serotonin; D008995:Monoamine Oxidase; D007099:Imipramine