Adrenergic, serotoninergic, histaminergic, and imipramine binding sites in post-mortal human cerebral microvessel preparations

1988 ◽  
Vol 73 (3) ◽  
pp. 177-189 ◽  
Author(s):  
C. O'Neill ◽  
C. J. Fowler ◽  
J. O. Marcusson ◽  
B. Winblad
1987 ◽  
Vol 12 (3) ◽  
pp. 193-198 ◽  
Author(s):  
D.H. Desmedt ◽  
D. Egrise ◽  
J. Mendlewicz

1988 ◽  
Vol 46 ◽  
pp. 236
Author(s):  
Ritsuko Takano ◽  
Toru Egashira ◽  
Yasumitsu Yamanaka

1991 ◽  
Vol 6 (2) ◽  
pp. 73-78
Author(s):  
G Faludi ◽  
K Tekes

SummaryDensity (Bmax) and affinity constant (Kd) values of tritiated imipramine binding sites were determined on platelets from patients suffering from major depression and from healthy, age-and sex-matched controls. Significantly lower Bmax values were found in the depressed patients, while the Kd values did not differ from those of controls. The results suggest that, in accordance with data from the literature, decrease in 3H-imipramine binding sites may be used as a state-dependent biological marker of depression in clinical practice.


1990 ◽  
Vol 189 (2-3) ◽  
pp. 175-183
Author(s):  
Andrey M. Fomenko ◽  
Yury G. Plyashkevich ◽  
Oleg S. Brusov ◽  
Vladimir P. Demushkin

1984 ◽  
Vol 4 (7) ◽  
pp. 755-771 ◽  
Author(s):  
Marta Stockert ◽  
Angela Veiga ◽  
Sergio Butman ◽  
Eduardo De Robertis

1981 ◽  
Vol 317 (4) ◽  
pp. 310-314 ◽  
Author(s):  
G. Gro� ◽  
M. G�thert ◽  
H.-P. Ender ◽  
H.-J. Sch�mann

1983 ◽  
Vol 142 (2) ◽  
pp. 188-192 ◽  
Author(s):  
E. K. Perry ◽  
E. F. Marshall ◽  
G. Blessed ◽  
B. E. Tomlinson ◽  
R. H. Perry

SummaryThe binding of tritiated imipramine was significantly reduced in the hippocampus and occipital cortex from a series of patients with depressive illness compared with age-matched patients with no psychiatric disorder. In contrast there was no change in imipramine binding in established cases of senile dementia of Alzheimer-type. Scatchard analysis indicated normal binding affinity but a reduction in the number of imipramine binding sites in depression. These observations parallel previous findings of decreased binding sites in platelets from depressed patients and suggest there may be an abnormality in the uptake mechanism for serotonin in depression.


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