Biomedical subjects

R Beeston

Publications and source records attributed to R Beeston.

5 recordsLinked to original sources

PubMed1992

Platelet imipramine binding is increased in essential thrombocythaemia.

A decrease in platelet serotonin content is well recognized in myeloproliferative disorders, although the basis for this is unclear. The relationship between decreased platelet serotonin and the number of serotonin transport channels in the platelet membrane was explored indirectly by measuring the number of the closely associated imipramine binding sites. Imipramine binding parameters were determined in 12 patients suffering from either essential thrombocythaemia or polycythaemia rubra vera and in 10 healthy controls. The maximal number of imipramine binding sites (Bmax) was increased in both patient groups, significantly so in those suffering from essential thrombocythaemia. This increase contrasts with a decrease in binding in other conditions known to be associated with decreased platelet serotonin. This study thus demonstrates a discrepancy in terms of reduced platelet serotonin content and increased imipramine binding on platelets from patients suffering from essential thrombocythaemia. It is suggested that further investigation of the imipramine binding site in these disorders, in parallel with measures of platelet serotonin content and uptake, is warranted.

Adult↗

PubMed1992

Platelet 3H-imipramine binding during recovery from depression.

Decreased binding of tritiated imipramine to platelets has been considered to be a potential biological marker of depression. However, it has been unclear how binding values alter during treatment and recovery. This study investigated imipramine binding parameters and depressive symptoms in 25 patients suffering from major depression at entry to the study and 1, 3 and 6 months later. Although the initial Bmax values were significantly lower in the depressed patients than in healthy subjects, it was not possible to establish a clear relationship between recovery from depression and Bmax. The power of this study to detect an effect of at least 10% of the variance in Bmax due to factors related to recovery from depression was 0.78.

Adult↗

PubMed1991

Platelet tritiated imipramine binding in patients suffering from mania.

Platelet imipramine binding was measured in 16 patients suffering from DSM-IIIR mania and compared with binding values reported in depressed and healthy control subjects recruited in a parallel study (Ellis et al., 1990). Binding levels in the manic group did not differ from control values, but were higher than in the depressed group. Within the manic group, binding did not differ with severity of illness or the presence of depressive symptoms but there was a trend to lower values (comparable to those in the depressed group) with increasing duration of illness. This raises the possibility that changes in imipramine binding in depression and mania may be similar, consistent with the permissive hypothesis of serotonin function.

Bipolar Disorder↗

PubMed1991

Circadian variation in platelet imipramine binding during the day in healthy subjects.

Platelet tritiated imipramine binding values in healthy controls vary considerably from study to study. A possible contributor to such variation might be a circadian rhythm affecting binding, although previous studies of this have been contradictory. Platelet imipramine binding was examined in 12 healthy, medication-free subjects studied at 8 a. m., 11 a. m., 4 p. m., and 10 p. m. during one day. Imipramine binding was determined on platelet membranes, using 0.8-8 nM 3H-imipramine, and nonspecific binding was defined by 50 microM desipramine. All samples from a given individual were assayed simultaneously. The intra-assay coefficient of variation was 6.3 percent. There was no evidence of significant differences in binding capacity or affinity (Bmax or Kd) at different times of day. Circadian variation was explored using COSINOR analysis (DeMet et al., 1989). There was no evidence of circadian variation in binding using this model, even when only the variable portion of binding was considered for each individual. Intraindividual variation in binding was substantial, with a mean coefficient of variation of 29 percent for Bmax and 38 percent for Kd. The possible basis of this variation is unclear, but may reflect the presence of "occult" binding sites in the membrane, or the effect of endogenous modulators of binding. The interrelationship of Bmax and Kd may also be a factor. It was considered that low-affinity binding did not account for a significant part of the variation in Kd in this assay. The utility of imipramine binding as a biological marker of depression may be limited by such levels of intraindividual variation in binding parameters.

Adult↗

PubMed1990

Platelet tritiated imipramine binding in psychiatric patients: relationship to symptoms and severity of depression.

The clinical and research significance of reduced imipramine binding has remained unclear despite considerable investigation. This study used an assay of demonstrated reliability to investigate the clinical correlates of imipramine binding to platelets in 63 depressed and 33 nondepressed psychiatric patients and 40 healthy control subjects. Both patient groups had Bmax values significantly lower than those of the healthy controls. Unequivocal associations between binding parameters and individual symptoms or groups of symptoms were not established, but a negative correlation between Kd and the number of adverse life events experienced in the preceding 6 months was apparent. These findings provide no support for the view that reduced binding is a trait marker for susceptibility to depression and cast doubt on its specificity as a state marker for the syndrome of depression.

Adult↗