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We studied the distribution of aromatic L-amino acid decarboxylase (AAAD) activity in striatal compartments of rats. After near-total destruction of nigrostriatal dopaminergic neurons, 15 to 20% of the initial enzyme activity remained. Striatal enzyme activity remained unchanged after destruction of serotoninergic terminals by electrolytic raphe lesions. Combined raphe-nigrostriatal lesions or nigrostriatal lesions alone produced similar decreases in striatal decarboxylase. Intrastriatal injection of kainic acid (which selectively destroys striatal interneurons and efferent neurons and also induces marked glial proliferation) reduced activity by 20%. Only 7% of initial striatal activity (perhaps localized in capillaries) remained after combined nigrostriatal-kainic acid lesions. These findings indicate that after degeneration of dopaminergic terminals, striatal interneurons and efferent neurons, but not serotonergic terminals of glia, contain an important fraction of the residual AAAD. This compartment may be the site of enzymatic conversion of exogenous L-dopa to dopamine in the parkinsonian striatum.

To examine the possibility that long-term L-DOPA therapy may be toxic to and destroy nigrostriatal dopaminergic neurons, mice were given large doses of L-DOPA (200 mg per animal per day) for 18 months. L-DOPA treatment was then discontinued to allow washout of drug from brain; 8 days later, L-DOPA was undetectable in corpora striata. Biochemical indices of the integrity of nigrostriatal neurons (striatal dopamine and DOPAC concentrations and activities of tyrosine hydroxylase and DOPA decarboxylase) were equal in DOPA-treated and control mice, suggesting that prolonged L-DOPA administration did not damage nigrostriatal neurons.

Administration of the pineal hormone melatonin (MEL) lowers serum gonadotropin (GN) levels, delays sexual maturation and elicits gonadal atrophy in rodents. In humans an antigonadotropic effect of the pineal has been sought for many years. Recently we reported higher nocturnal serum MEL levels in prepubertal children than in young adults. Now we have examined the immediate effects of exogenous MEL on basal levels of various hormones. After giving informed consent 5 healthy, male adolescents received 80 mg oral MEL at 11:00; 3 volunteers received the same dosis at 11:00,12:00 and 13:00. Serum concentrations of MEL, GN, testosterone (T) and prolactin (PRL) were determined at 30-min. intervals several hours prior to, during, and after MEL administration. Though serum MEL concentrations increased at least 1000 times above basal levels GN and T were not altered. PRL rose from 4.6±0.7 (x±SEM) to 7.6±0.9 ng/ml (p

Compositions containing controlled amounts of d,l-fenfluramine are administered to block the intermittent carbohydrate cravings without necessarily suppressing other food intakes.

THE mammalian pineal gland has the unique ability to synthesize methoxyindoles such as melatonin1,2 and methoxytryptophol3. It has been suggested that these compounds function as hormones4,5: melatonin is secreted into the circulation4,6 and efficiently extracted from the blood by most tissues7,8; both compounds inhibit gonad function4,5,9, and it has also been claimed that melatonin acts on the thyroid10,11, gut12, pituitary13, skin14 and brain15.

Excerpt Dr. Robert A. Cohen: On previous occasions when our Institute has had the responsibility for presenting one of these Combined Clinical Conferences I have considered it almost an obligation ...

Oxidative processes in schizophrenia are currently being studied in many laboratories because some authors have speculated that hallucinations and other symptoms of schizophrenia might be caused by substances produced during possibly abnormal oxidation of epinephrine in schizophrenic patients. Akerfeldt 1 recently described a test that measures the oxidative power of serum; this test depends on the time that it takes for a red color to appear in serum after the addition of N,N'-dimethyl- p phenylenediamine, a substance that turns red when oxidized. Akerfeldt reported that serum from schizophrenic patients oxidized this substance very rapidly, whereas serum from normal subjects oxidized it slowly. However, he also noted that both normal pregnancy and chronic infection likewise caused abnormally rapid oxidation of N,N'dimethyl- p -phenylenediamine. Nevertheless, some observers have accepted the test as useful in the diagnosis of mental disease. On the other hand, Horwitt et al. 2 found the test to be without value, and Angel et al. 3