[Biochemical methodology for studying affective disorders]

Defects in brain neurotransmitter function are believed to be involved in the aetiology of mood disorders, and model systems are based on this concept. Abnormalities in synthesis, storage, release, reuptake or catabolism of monamines, GABA, glycine, taurine, peptides and purines may occur. There may also be an endogenous psychotogen--an aberrant metabolite of a transmitter. Models are divided into two groups. 1. Human. Brain, CSF, blood cells (platelets, erythrocytes), plasma and urine have been analysed for neurotransmitters or metabolites. Particular emphasis has been given to serotonin (5-HT) and the catecholamines, dopamine and noradrenaline. 2. Animal. Human mood disorders may be stimulated by drug-induced behavioural changes in animals (hyperactivity, stereotyped behaviour sedation). The above biochemical parameters relating to neuronal function can then be assessed. Brain neuronal pathways can be stimulated in animals with monoamine precursors and MAO inhibitor drugs. This drug-induced hyperactivity can be used to "evaluate" therapeutic techniques such as electroconvulsive therapy (ECT). Model analogues of mood disorder have limited use until human disease aetiology is known, currently the best use of models may be for demonstration and evaluation of particular similarities between human mood disorders and drug-induced alterations of animal behavioural patterns.