Abstract
There is evidence to show that blood platelets possess a similar serotonergic mechanism (uptake, storage and release) to the nerve-endings of the serotonin-containing neurons of the central nervous system. Parallel studies were therefore carried out on the effects of malnutrition on the serotonin metabolism in both synaptosomes and the blood platelets in an attempt to validate the use of blood platelets as a model for central neuronal serotonin transmission, especially in children suffering with protein-energy malnutrition (PEM). The nutritional status of growing rats was manipulated by feeding them a low protein (3% casein) diet. Litter mates were pair-fed restricted amounts of a high protein (25% casein) isocaloric diet. Controls were allowed unrestricted access to the high protein diet. These manipulations made it possible to study the effects of low protein intake, ie, malnutrition and low energy intake, i.e., undernutrition on serotonin metabolism. Platelets were obtained from platelet-rich plasma (PRP) prepared from blood taken by cardiac puncture of slightly anaesthetized male Wistar albino rats; the synaptosomes were derived by differential and discontinuous sucrose density gradient centrifugations of the brains. The diet-induced steady states of tryptophan (TP), 5-hydroxytryptamine, 5-HT (serotonin) 5-hydroxyindole acetic acid (5-H1AA) and 3H-TP uptake into the respective tissue proteins were investigated. The protein content of each tissue was also determined. The results (expressed as a ratio to protein) showed that although the blood platelets bear a high degree of similarity in TP concentrations and uptake to central synaptosomes, especially in young rats, this similarity was not apparent in older animals. The results showed in particular that malnutrition had no effect on the serotonin concentration in the synaptosomes. Whereas this was highly distorted in the platelets from both malnutrition and undernourished animals. The formation of 5-H1AA, though distorted in nutritionally-deprived platelets, was similar to the controls. The blood platelets were more vulnerable to a dietary deficiency of protein than of energy. This was evident in the higher levels of TP, 5-HT and 5-H1AA and lower protein content in the platelets of the protein-deficient animals. It was concluded from the results that in rats the blood platelet is not a suitable model for central neuronal serotonin transmission in nutritionally-deprived animals. Moreover, the fact that there was a difference between the concentration of serotonin in the blood platelets and synaptosomes, probably indicating dissimilarities in uptake, storage and release, in the control animals may preclude the use of platelets as a model for central synaptic serotonin metabolism, even in physiological conditions. However, it may be that blood platelets could be useful in assessing nutritional status.