J. Disselkamp-Tietze

Bio: J. Disselkamp-Tietze is an academic researcher from University of Würzburg. The author has contributed to research in topics: Receptor & Ipsapirone. The author has an hindex of 1, co-authored 1 publications receiving 72 citations.

5-HT1A receptor function in depression : effect of chronic amitriptyline treatment

Abstract: Hypothermic responses to 5-HT1A receptor activation by the selective ligand ipsapirone (IPS) were attenuated in depressed patients as compared to controls. Chronic treatment with amitriptyline (AMI) further impaired 5-HT1Amediated hypothermia. The results indicate a subsensitive (presynaptic) 5-HT1A receptor and/or a defective post-receptor signalling pathway in depression and are consistent with the hypothesis that 5-HT1A receptors are down-regulted during AMI treatment.

Serotonin and the neurobiology of depression. Effects of tryptophan depletion in drug-free depressed patients.

Abstract: Objective: To investigate the effects of tryptophan depletion in untreated depressed patients. Rapid dietary depletion of the precursor of serotonin synthesis, tryptophan, causes a transient return of depression in 67% of patients who have had a therapeutic antidepressant response. Method: Forty-three untreated depressed patients underwent tryptophan depletion in a double-blind, placebocontrolled cross-over study. After testing, they received open sequential antidepressant treatment. Results: Mood did not change when tryptophan was depleted but did change on the day after the depletion test. Relative to the control test, 37% of the patients had 10-point or greaterdecreasein Hamilton Depression Rating Scale (Ham-D) score, while 23% had a 10-point or greaterincreasein Ham-D score on the day after the tryptophan depletion test. Change in mood was correlated to treatment response after testing. Patients whose condition worsened proved to be highly refractory to treatment while those who showed improvment were more likely to respond. Conclusions: That tryptophan depletion did not rapidly worsen depression argues that serotonin function is not linearly related to the level of depression and if reduced serotonin function does cause depression, then it is either as predisposing factor or due to a postsynaptic deficit in the utilization of serotonin.

Gene–environment interaction and the genetics of depression

Abstract: Depression is a group of brain disorders with varied origins, complex genetics and obscure neurobiology. Definitions of clinical phenotypes are not rooted in their neurobiology, and animal models of behavioural despair have considerable limitations. Nevertheless, investigation of subtle alterations in gene expression, of correlations between genotype and brain activity, and of environmental variables interacting with genetic variants have advanced research into the genetics of depression. Although the postgenomic era is still in its infancy, several milestones have already been reached: variation in gene expression has been confirmed to play a predominant role in individual differences; gene-environment interactions have been established in humans and in a nonhuman primate model; gene-phenotype correlations have been substantiated by functional neuroimaging; and the notion of gene networks that control brain development is increasingly recognized. Given the etiologic and psychobiologic complexity of mood disorders, it is not surprising that the identification of specific genetic factors is extremely difficult and continues to be among the last frontiers of gene hunting.