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Mental disorders affect a high percentage of the general population and are associated with a significant burden. One major component of treatment for mental illnesses is pharmacotherapy. Various psychotropic medications are used in the treatment of psychiatric disorders and these are often associated with a plethora of side effects. The many side effects of psychotropic drugs can severely impair patients’ quality of life and decrease their adherence to treatment. Among the relatively neglected and less-studied potential side effects of psychotropic drugs are impairment of sperm parameters and fertility problems among male patients. This article summarizes the data with regard to the effects of 6 widely used psychotropic drugs—lithium, valproate, haloperidol, olanzapine, imipramine, and fluoxetine—on sexual function and sperm parameters in male subjects. In general, the reviewed data suggest that these medications can be associated with sexual function problems and negative effects on sperm parameters among male subjects. It is important to note that most of the data are based on preclinical studies and nonrandomized clinical trials with relatively small sample sizes, so that it is not possible to draw unequivocal conclusions with regard to the clinical relevance of the findings. Prospective, randomized clinical trials are necessary to elucidate the effects of psychotropic drugs on men’s sperm parameters and fertility indices per se.

Olanzapine (OLZ) is an atypical antipsychotic drug that also has mood-stabilizing effects. The mechanism of action of OLZ is not fully understood. Accumulating data suggest that inflammation plays a role in the pathophysiology of mental disorders and that psychotropic drugs exhibit some anti-inflammatory properties. This study was undertaken to examine the effects of OLZ on LPS-induced inflammation in rat primary glia cells. Glia cells were extracted from newborn rat brains. OLZ (1 or 50 µM) was added to culture medium at 6 or 72 h before addition of LPS for another 18 h, and levels of IL-10, prostaglandin (PG) E2, NO and TNF-α, and expression of cyclo-oxygensase (COX)-2 and inducible NO synthase (iNOS) were determined. Treatment with 50 µM OLZ (but not 1 µM) significantly decreased LPS-induced secretion of IL-10, PGE2and TNF-α. In contrast, 50 µM OLZ significantly increased NO levels. OLZ did not alter the expression of COX-2 or iNOS in LPS-treated cells. These results suggest that OLZ differently affects the secretion of inflammatory mediators. Most of the significant effects of OLZ were obtained when 50 µM was used, which is a high and probably therapeutically irrelevant concentration. Therefore, under the conditions used in the present study OLZ seemed to lack a potent anti-inflammatory effect.

Several studies of normobaric hyperoxia in neurological conditions have found positive results. The impaired energy metabolism due to mitochondrial dysfunction and frontal lobe hypofunction in schizophrenia might be improved by increasing O2supply to the brain. Normobaric hyperoxia may be a potential treatment for schizophrenia. Participants in this study, outpatients with chronic schizophrenia and inhabitants of community-based psychiatric institutions (hostels), underwent baseline psychiatriccognitive assessment and were randomly assigned to either a treatment intervention of oxygen-enriched air inhalation (normobaric hyperoxia of 40 fraction of inspired oxygen) or regular air inhalation (21 fraction of inspired oxygen), through a nasal tube, for 4 weeks. Patients were given the airoxygen inhalations during the night (mainly while sleeping) for at least 7 hours a night. After completing 4 weeks of treatment, patients were switched (crossed over) to the other treatment intervention. Fifteen patients completed the entire study. Five additional patients completed phase A only. There was significant improvement in total Positive and Negative Symptoms Scale score of patients who received oxygen compared with the control group. There were positive effects of oxygen on memory and attention in neuropsychological performance tests. The effect size is small despite the statistical significance, but the patient group was extremely chronic and severely impaired. These results are a proof of concept, and normobaric hyperoxia should be studied in patients with milder forms of the illness and earlier in the course of illness.

Bipolar disorder is a severe and chronic illness affecting approximately 1.5% of the American population. Despite the availability of mood bipolarstabilizers such as lithium, valproate, carbamazepine and lamotrigine, bipolar disorder is characterized by high rates of recurrence, as treatment with these and other drugs is ineffective for and not tolerated by a significant percentage of patients. Several hypotheses have been postulated to explain the mechanism(s) of action of mood stabilizers. However, the biological and molecular bases of the disease are not fully understood, hampering the development of more effective and safer drugs. A large body of evidence associates lipids (cholesterol, phospholipids and fatty acids) with the mechanism and pathology of bipolar disorder. The purpose of this paper is to review the lipid connection to bipolar disorder.

There is a growing body of evidence suggesting that vagal afferents play a major role in peripheral-neural communication. This study was undertaken to determine whether a dose-dependent effect of lipopolysaccharide (LPS) on vagotomy-induced febrile unresponsiveness exists, and to examine the effect of vagotomy on LPS-induced increase in hypothalamic prostaglandin E2(HT PGE2) production. Vagotomized and sham-operated rats were subjected to two experimental protocols. In the first, vagotomized and sham-operated rats were injected intraperitonealy with different doses of LPS (200, 500 and 1000 µg/kg) in order to examine the dose-dependent effect of LPS on the biphasic febrile response of the rats. In the second protocol, vagotomized and sham-operated rats were injected intraperitonealy with LPS (500 µg/kg). Two hours post injection, body temperature was measured, the rats were decapitated and blood was collected. Simultaneously, the rats' hypothalami were excised and incubated for 1 h in a Krebs-Henseleit buffer. Next, HT PGE2was determined by radioimmunoassay. Vagotomy-induced gastric enlargement was then measured to examine the correlation between the magnitude of the enlargement and that of the vagotomy-related febrile unresponsiveness. It was found that vagotomized-induced febrile unresponsiveness is a dose-dependent effect. Subdiaphragmatic resection of the vagus prevented the biphasic febrile response caused by the lowest dose (200 µg/kg) of LPS, whereas the highest dose of LPS (1000 µg/kg) caused a similar biphasic febrile response in both vagotomized and sham-operated rats. Indeed, vagotomy attenuates LPS-induced increase in HT PGE2, and blocks the hypothermic phase of the febrile response. On the other hand, no correlation between gastric enlargement and febrile unresponsiveness was found. The results of the present study may cast further light on the crucial role of the vagus nerve as a peripheral-neural pathway in the mediation of the febrile response.