Following SSRI therapy, brain serotonin turnover was substantially reduced (mean internal jugular venoarterial 5-hydroxyindoleacetic acid plasma concentration difference, 6.0 nmol/L prior to treatment vs 2.0 Analysis of the influence of the 5-HTT genotype in MDD indicated that carriage of the s allele compared with the l allele was associated with greater than a 2-fold increase in brain serotonin turnover (mean internal jugular venoarterial 5-hydroxyindoleacetic acid plasma concentration difference, 6.5 vs 2.7 nmol/L, Results Brain serotonin turnover was significantly elevated in unmedicated patients with MDD compared with healthy subjects (mean internal jugular venoarterial 5-hydroxyindoleacetic acid plasma concentration difference, 4.4 vs 1.6 nmol/L, respectively P = .003). Main Outcome Measures Brain serotonin turnover before and after SSRI therapy. Interventions Treatment for patients consisted of SSRI administration for approximately 12 weeks. Participants Studies were performed in 21 patients fulfilling the DSM-IV and International Statistical Classification of Diseases, 10th Revision diagnostic criteria for MDD and in 40 healthy volunteers. Experimental procedures were performed in the research catheterization laboratory of a major training hospital and medical research institute. Setting Participants were recruited from the general community following media advertisement. The effect of serotonin transporter (5-HTT) genotype on brain serotonin turnover was evaluated and the influence of SSRI therapy on serotonin turnover was investigated. Direct internal jugular venous blood sampling was used to directly quantify brain serotonin turnover. Healthy volunteers were examined on only 1 occasion. In an unblinded study of sequential design. Objective To quantify brain serotonin (5-hydroxytryptamine ) turnover in patients with MDD.ĭesign Patients with depression were studied both untreated and during administration of a selective serotonin reuptake inhibitor (SSRI) Shared Decision Making and CommunicationĬontext The biological basis for the development of major depressive disorder (MDD) remains incompletely understood.Scientific Discovery and the Future of Medicine.Health Care Economics, Insurance, Payment.Clinical Implications of Basic Neuroscience.Challenges in Clinical Electrocardiography.Vesicular serotonin transport occurs via the action of the vesicular monoamine transporter.Īlterations in vascular permeability, which is influenced by the sympathetic nervous system, 8, 9 may influence the dynamics of capillary exchange and appearance of 5-HIAA in plasma. The availability of serotonin for intraneuronal metabolism is dependent on the balance between serotonin release (c) and the entry of serotonin into the axoplasm via the processes of intraneuronal reuptake (d)Īnd leakage (e) and removal (f) from the axoplasm. In cerebrospinal fluid, 5-hydroxyindoleacetic acid (5-HIAA) concentrations are approximately 200 times that of serotonin, 7 thereby rendering 5-HIAA levels an approximation of serotonin turnover. At steady state, the rate of serotonin synthesis (a) by definition must equal the rate of serotonin turnover, where turnover is equal to the sum of the rates of spillover of serotonin to plasma (b) and intraneuronal metabolism of serotonin (g).
doi:10.4088/JCP.Diagrammatic representation of the relative contributions to intraneuronal serotonin (5-hydroxytryptamine ) turnover. Depression: The case for a monoamine deficiency. Challenging the public stigma of mental illness: A meta-analysis of outcome studies. Biogenetic explanations and stigma: A meta-analytic review of associations among laypeople. Journal of Consulting and Clinical Psychology. Fixable or fate? Perceptions of the biology of depression.
Exces de serotonina update#
Antidepressants and the Chemical Imbalance Theory of Depression: A Reflection and Update on the Discourse. Behavioral Neurobiology of Depression and Its Treatment. Rockville (MD): Agency for Healthcare Research and Quality (US) 2007. Comparative Effectiveness of Second-Generation Antidepressants in the Pharmacologic Treatment of Adult Depression. Gartlehner G, Hansen RA, Thieda P, et al. Mitochondria and mood: Mitochondrial dysfunction as a key player in the manifestation of depression. The Jackson Laboratory.Īllen J, Romay-Tallon R, Brymer KJ, Caruncho HJ, Kalynchuk LE. Happy or SAD: The chemistry behind depression. Philosophical Transactions of the Royal Society B: Biological Sciences. The neurobiology of depression-revisiting the serotonin hypothesis.
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