Cerebrospinal fluid 5-hydroxyindoleacetic acid levels were determined in 31 women with unipolar involutional depression using the probenecid technique. Values were found to be lower in depression as compared to controls, but they did not correlate with the severity of the clinical picture. Anxiety, insomnia and drug response however showed significant correlation with pretreatment 5-HIAA level. Some possible interpretations are discussed.

5-Hydroxytryptamine (5HT, serotonin) content of the whole blood has been measured in hospitalized groups of manic, depressed, schizophrenic and alcoholic patients; values were compared to non-psychotic controls. Only depressives had significantly different values. Alcoholics occupied an intermediate position between depressives and controls. Schizophrenics had virtually the same average level. Manic patients showed a very weak tendency toward higher values. Neuroleptic drugs in mania did not alter the blood 5HT levels, but in depression tricyclic antidepressants caused an elevation after 3 weeks of treatment. These post-treatment levels no longer differed significantly from those of non-psychotic controls.

The effect of 1 mg dexamethasone on CSF levels of 5-hydroxyindoleacetic acid (5 HIAA), homovanillic acid (HVA) and cortisol (CS) was investigated in 100 psychiatric inpatients: 45 subjects had their lumbar punctures 1-4 days following dexamethasone administration, and the results were compared with those from 55 other patients investigated before drug ingestion. All patients were women, and none had received psychotropic medication for at least two weeks before the study. Seven subjects consented to two LPs both before and after dexamethasone. As expected, cortisol in the CSF significantly decreased after dexamethasone: the decrease was greatest 10 hours following the drug. HVA showed a weak and transient elevation after 10 hours only. CSF 5 HIAA was found to be significantly increased in postdexamethasone samples and high levels were still found even after 82 hours. Diagnostic differences (major or minor depression, schizophrenia, alcohol abuse or dependence) did not account for the observed differences. Repeated CSF examinations in seven subjects corroborated these findings: all cortisol values were decreased and all 5 HIAA values were increased after dexamethasone while HVA values showed random changes. The data may suggest that serotonergic mechanisms may be involved in dexamethasone action in the CNS. In addition, dexamethasone administration can alter CSF 5 HIAA level, a possible factor which should be taken into consideration in CSF studies.

No abstract

We examined the effects of the serotonin antagonist pizotifene (4 mg daily for 3 days orally), and the opiate antagonist naloxone-HCI (0.8 mg intravenously) on the TRH-induced thyrotropin (TSH), growth hormone (GH), and prolactin (PRL) response in female psychiatric inpatients with adjustment disorder or alcohol abuse. All the patients were free from interfering endocrine and metabolic illness and had not received major psychotropic medication before the investigation. Pizotifene caused a small but significant decrease of the TRH-induced TSH response in 8 patients, two of them changed their responses from normal (i.e. above 5 mU/l) to blunted. Neither GH nor PRL changed significantly after pizotifene. Naloxone-HCI, 30 min before the TRH challenge, did not produce any significant change in the TSH, GH or PRL responses, nor did it cause any significant change in the plasma level of these hormones by itself. The hormonal responses to TRH remained unaltered in ten other patients who had repeated tests without any drug treatment between the two occasions. The results suggest that serotonin deficiency may play a role in the blunted TSH response to TRH, while opiate mechanisms do not appear to have a primary influence on these endocrine effects of TRH.