The depressive patients can be divided into two subgroups by presence and absence of pain symptoms. Those without pain symptoms have blunted pain sensitivity whereas those with pain have normal range of pain sensitivity, and are clinically characteriz...
The depressive patients can be divided into two subgroups by presence and absence of pain symptoms. Those without pain symptoms have blunted pain sensitivity whereas those with pain have normal range of pain sensitivity, and are clinically characterized by anxiety and irritability.
The aim of the study is to test if these clinical profiles of the depressives with pain symptoms are related with reduced level of brain serotonin(5-HT).
Forty four mice were randomly divided into two groups : one group to be bred with tryptophan free diet and the other with normal control diet, each for 4 weeks. Before the beginning of the breeding period, measured were locomotor activity by open field test, anxiety by elevated plus maze and nociceptive sensitivity by tail flick test, before and after forced swimming(FS). During each FS, duration of immobilization was also measured. The sable sets of measurements were repeated at the end of the breeding period. The brain 5-HT and 5-hydroxyindoleacetic acid(5-HIAA) were measured by high performance liquid chromatography.
The results were as follows
1.Four weeks of tryptophan free diet reduced significantly body weight, brain weight, and levels of 5-HT and 5-HIAA in the whole brain.
2.Tryptophan depletion did not influence basal nociceptive sensitivity as measured by tail flick latency before FS. The normal blunting of the pain sensitivity induced by forced swimming was preserved in the tryptophan depleted group.
3.Tryptophan depletion did not influence general locomotor activity in open field.
4.Tryptophan depletion increased significantly time spent on the open arms at the elevated plus maze test done before FS. This anxiolytic-like effect was reduced by FS.
5.Tryptophan depletion did not influence duration of immobilization during FS.
From these results, it is suggested that the genesis of the depression with pain symptoms is not medicated by quantitative reduction of brain serotonin