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By using phase-contrast microscopy combined with a fluorescent staining technique, the frequency of blast-type atypical lymphocytes (BTALs) appearing in peripheral blood and the phenotypic expression of their surface antigens were studied in 24 patients with schizophrenia, 16 with mood disorder and 14 healthy controls. BTALs were classified as being stimulated or activated cells, morphologically characterized by their large size, dark cytoplasm, a hollow perinuclear containing a few granules and finely dispersed chromatin structures with a few evident nucleoli. A significantly higher number of BTALs were found in the schizophrenic patients compared with healthy control subjects or patients with mood disorder. Further, there was a significant difference in the frequency of BTALs between patients with mood disorder and healthy control subjects. No significant difference in the frequency of BTALs was found between the schizophrenic patients with and without medication. Immunostaining of BTALs revealed that these cells consisted of B, T and non-B, non-T cell subpopulations. Contrary to our expectations, the T cell was only one third of the BTAL population. HLA-DR and CD38 were expressed on most BTALs (> 70%), while CD25, an early activation marker of T cells was rarely found on BTALs (< 0.3%). The differences in activated lymphocyte populations which appeared as morphologically atypical in the circulation among some psychiatric patients and infectious or autoimmune diseases are discussed. This is the first report on populations of BTALs.

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Reviewing the development of concepts of 'atypical' psychoses in European countries and in the United States shows that there are various terminologies which are given to a group of psychoses unclassifiable within Kraepelinian dichotomy. Bouffée délirante (French school), cycloid psychoses (Leonhard, Perris), reactive psychoses (Scandinavian school) and acute schizoaffective psychoses (Kasanin) are the most common terms. These are consistent in terms of acute onset, polymorphic symptomatology and good prognosis, and are considered to be distinct from major psychoses, especially from typical schizophrenia. The concept atypical psychoses in Japan was developed under the influence of Mitsuda's clinico-genetic studies. According to Mitsuda, atypical psychoses are not mere phenotypical variants of typical schizophrenia and manic-depressive psychosis (MDP) but belong to a genetically different category and are probably heterogeneous. The characteristic features in the Japanese concept of atypical psychoses emphasizes the alteration of consciousness in symptomatology and pays attention to the nosological relationship with epilepsy, as well as with schizophrenia and MDP. Thus, in Japan it is generally considered that atypical psychoses are independent of 'typical' major psychoses and are located nosologically in the border area between typical schizophrenia, MDP and epilepsy.

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Le(y) is a carbohydrate determinant of membrane glycoconjugates and is expressed in some tumor and embryonic cells. On T lymphocytes, it is known that human immunodeficiency virus (HIV)-infected human lymphocyte T-cell lines express elevated Le(y) antigen and AIDS patients show the highest Le(y) expression in T lymphocytes at lower CD4/CD8 ratio. Later, a comparative elevation of Le(y) expression on T-cell subsets has been noticed to be mainly present in patients with viral diseases, such as acute and chronic hepatitis, implying an association of the highest Le(y) expression with viral infection. We found that Le(y) antigen was most expressed in both CD4+ and CD8+ subsets of peripheral T lymphocytes in hospitalized schizophrenic patients. On the other hand, atypical lymphocytes with stimulated morphology are known to appear in the blood circulation of schizophrenic patients. Similar atypical lymphocytes have also been described in viral and autoimmune diseases. Two possibilities have been discussed: viral association in the pathology in some schizophrenic patients; and immunological abnormalities including environmental effects under hospitalization on immune status, since normal controls (staff in psychiatric hospitals) showed higher Le(y) expression than normal controls under non-psychiatric circumstances.

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Forced running stress induced a prolonged inactive state with the abolition of hormone-dependent cyclic behavior in some female rats which had already recovered from physical exhaustion. The state could be regarded as a "depression model" in these animals. In the biochemical study, norepinephrine in the hypothalamus was found to be significantly lowered in these animals. In the histochemical study, an increase of fluroescence intensity in nerve cell groups of the ascending norepinephrine system and a decrease of fluorescence intensity in nerve cells and terminals of the tubero-infundibular dopamine system were found in these animals. These findings were also seen in the rats which were examined immediately after the stress, but not in the rats which recovered their spontaneous and cyclic running activity in several weeks after the stress. These results suggest that changes of monoamine metabolism in the brain which is induced by the stress remains unrestored for a long time in the "depression model rats".

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Nineteen out of 51 depressed patients showed abnormal TSH response to TRH in terms of exaggerated, diminished and delayed responses. The basal value of T3 and its response to TRH were significantly lower in patients with delayed or diminished response than in the normal subjects. These results indicate that the dysfunction of the hypothalamo-pituitary thyroid axis plays an important role in the pathogenesis of depression.

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A number of cases of depressed patients have latent hypothyroidism, possibly due to hypothalamo-pituitary dysfunction, and become refractory to antidepressant drugs. The dramatic effect or thyroid medication combined with tricyclic antidepressants is often observed in such persistently depressed patients. This effect seems to pertain to the catecholamine hypothesis of depression, but this requires further elucidation.

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Changes in urea cycle enzymatic activities in the liver induced by intracerebral electrical stimulation in rabbits with chronically implanted electrodes in the hypothalamus, the thalamus, and the limbic area were studied in comparison with these activities in non-stimulated controls. In stimulating the ventromedial nucleus of the hypothalamus, the two-hour sessions were followed by significantly reduced activity in arginase and the arginine synthetase system in the liver, but the six-hour stimulation sessions were followed by normal range activity in these enzymes. In stimulating the lateral hypothalamic area, the two-hour sessions were followed by only slightly reduced activity in the arginine synthetase system in the liver. Stimulation of the center median nucleus of the thalamus, the medial area of the amygdala and the dorsal hippocampus produced no significant changes in urea cycle enzymatic activities in the liver. The possibility that ammonia metabolism in the liver may be modified through some functional linkage between the brain and the liver was suggested.

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