Someone recently bought our

students are currently browsing our notes.


Serotonin Depression Notes

Medicine Notes > Psychology Notes

This is an extract of our Serotonin Depression document, which we sell as part of our Psychology Notes collection written by the top tier of Oxford students.

The following is a more accessble plain text extract of the PDF sample above, taken from our Psychology Notes. Due to the challenges of extracting text from PDFs, it will have odd formatting:

1. Discuss the possible role of serotonin in the causes and treatment of depression Role of serotonin In cause of depression Serotonin hypothesis: Proposed by Alec Coppen - Diminished activity of 5-HT pathways plays a causal role in pathophysiology of depression Evidence:
-Coppen et al-1978: To show there was diminished activity of 5-HT in the CNS pathways - serotonergic transport in human platlets is used as a model due to similarities of processes in the central serotonergic neurons- Kinetic analysis using low substrate concentrations and measuring initial uptake rate have shown that uptake of 5-HT into platelets of depressed patients is decreased
-Changes in platelet uptake may be secondary and possibly compensatory to depression and chemical and hormonal changes
-Reduced CSF concentrations of 5-HIAA-major metabolite of 5-HT in drug free depressed patients, reduced concentrations in post-mortem brain tissue/suicidal patients, decreased plasma tryptophan concentrations
-Cowen et al: 1989 showed that there was decreased plasma tryptophan levels in major depression- need other risk factors
-Tryptophan depletion- lower plasma and brain tryptophan by administering an amino acid mixture free of 5-HT precursor tryptophan- in healthy volunteers, lowering tryptophan doesn't produce changes in mood- this suggests that lowering brain 5-HT is not sufficient to cause clinical depressive symptomatology (is this evidence against serotonin as not the major causative agent?). But in recovered depressed patients withdrawn from medication tryptophan depletion causes transient and striking return of depressive symptomatology
-Suggests that patients with risk factors for depression- lowering brain 5-HT function causes clinical depressive symptomatology
-The same finding is found when catecholamines are depleted with amethyl-para tyrosine-this shows recovered recovred depressed patients are psychologically vulnerable to both 5-H and Catecholamine deficiency
-Brain imaging techniques- ligand imaging with PET and single photon emission tomography- enables direct investigation of 5-HT receptors in living human brainthese data have provided consistent and convincing evidence that binding density of 5-H1a receptors show widespread decrease in depressed patients
-5-HT genes and depression: Depression in twins and families have shown moderate to high heritability

Buy the full version of these notes or essay plans and more in our Psychology Notes.