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Recent research into the rapid antidepressant effect of subanesthetic doses of ketamine have identified a series of relevant protein cascades activated within hours of administration. Prior to, or concurrent with, these activation cascades, ketamine treatment generates dissociative and psychotomimetic side effects along with an increase in circulating glucocorticoids. In rats, we observed an over 3-fold increase in corticosterone levels in both serum and brain tissue, within an hour of administration of low dose ketamine (10 mg/kg), but not with (2R, 6R)-hydroxynorketamine (HNK) (10 mg/kg), a ketamine metabolite shown to produce antidepressant-like action in rodents without inducing immediate side-effects. Hippocampal tissue from ketamine, but not HNK, injected animals displayed a significant increase in the expression of sgk1, a downstream effector of glucocorticoid receptor signaling. To examine the role conscious sensation of ketamine’s side effects plays in the release of corticosterone, we assessed serum corticosterone levels after ketamine administration while under isoflurane anesthesia. Under anesthesia, ketamine failed to increase circulating corticosterone levels relative to saline controls. Concurrent with its antidepressant effects, ketamine generates a release of glucocorticoids potentially linked to disturbing cognitive side effects and the activation of distinct molecular pathways which should be considered when attempting to delineate the molecular mechanisms of its antidepressant function.

Background Evidence continues to build suggesting that the GABAergic neurotransmitter system is altered in brains of patients with major depressive disorder. However, there is little information available related to the extent of these changes or the potential mechanisms associated with these alterations. As stress is a well-established precipitant to depressive episodes, we sought to explore the impact of chronic stress on GABAergic interneurons. Methods Using western blot analyses and quantitative real-time polymerase chain reaction, we assessed the effects of five-weeks of chronic unpredictable stress exposure on the expression of GABA-synthesizing enzymes (GAD 65 and GAD 67 ), calcium-binding proteins (calbindin, parvalbumin, and calretinin), and neuropeptides co-expressed in GABAergic neurons (somatostatin, neuropeptide Y, vasoactive intestinal peptide, and cholecystokinin) in the prefrontal cortex and hippocampus of rats. We also investigated the effects of corticosterone and dexamethasone exposure on these markers in vitro in primary cortical and hippocampal cultures. Results We found that chronic unpredictable stress induced significant reductions of GAD 67 protein levels in both the prefrontal cortex and hippocampus of chronic unpredictable stress-exposed rats but did not detect changes in GAD 65 protein expression. Similar protein expression changes were found in vitro in cortical neurons. In addition, our results provide clear evidence of reduced markers of interneuron population(s), namely somatostatin and neuropeptide Y, in the prefrontal cortex, suggesting these cell types may be selectively vulnerable to chronic stress. Conclusion Together, this work highlights that chronic stress induces regional and cell type-selective effects on GABAergic interneurons in rats. These findings provide additional supporting evidence that stress-induced GABA neuron dysfunction and cell vulnerability play critical roles in the pathophysiology of stress-related illnesses, including major depressive disorder.

Neuropsychiatric symptoms and mental illness are commonly present in patients with chronic systemic diseases. Mood disorders, such as depression, are present in up to 50% of these patients, resulting in impaired physical recovery and more intricate treatment regimen. Stress associated with both physical and emotional aspects of systemic illness is thought to elicit detrimental effects to initiate comorbid mental disorders. However, clinical reports also indicate that the relationship between systemic and psychiatric illnesses is bidirectional, further increasing the complexity of the underlying pathophysiological processes. In this review, we discuss the recent evidence linking chronic stress and systemic illness, such as activation of the immune response system and release of common proinflammatory mediators. Altogether, discovery of new targets is needed for development of better treatments for stress-related psychiatric illnesses as well as improvement of mental health aspects of different systemic diseases.

Exposure to extreme stress can trigger the development of major depressive disorder (MDD) as well as post-traumatic stress disorder (PTSD). The molecular mechanisms underlying the structural and functional alterations within corticolimbic brain regions, including the prefrontal cortex (PFC) and amygdala of individuals subjected to traumatic stress, remain unknown. In this study, we show that serum and glucocorticoid regulated kinase 1 (SGK1) expression is down-regulated in the postmortem PFC of PTSD subjects. Furthermore, we demonstrate that inhibition of SGK1 in the rat medial PFC results in helplessness- and anhedonic-like behaviors in rodent models. These behavioral changes are accompanied by abnormal dendritic spine morphology and synaptic dysfunction. Together, the results are consistent with the possibility that altered SGK1 signaling contributes to the behavioral and morphological phenotypes associated with traumatic stress pathophysiology.

Numerous studies have investigated the various consequences of traumatic experiences during the war. The most significant disorder that occurs as a result of war traumatization is posttraumatic stress disorder, in addition to which other psychological disorders often can occur. In the last few decades, the number of studies researching the occurrence of posttraumatic growth as a positive outcome of trauma, including that of war veterans, has been growing. Among war veterans, prisoners of war stand out for the intensity of their traumatic experience but also for the appearance and intensity of the pathological outcomes of the trauma. Studies show that in this group of veterans, posttraumatic stress disorder and comorbidity disorders often persist for decades after their release from captivity. There is not much research about the positive outcomes of trauma in these particularly vulnerable populations, and this paper is a review of several different studies, the results of which show that posttraumatic growth is possible even after challenging traumatic experiences such as war captivity.

Schizophrenia is a complex psychiatric condition that, if not adequately treated, can affect functional limitations. The exact etiopathogenesis of schizophrenia remains unknown. Research suggests an interaction between many factors, including genetic susceptibility, environment and psychological processes. Specific authors describe the association of a valuable mineral in the human body, iron, with pathophysiological mechanisms and related etiological factors in the development of the severe mental illness of schizophrenia. Iron has important roles in the human body and affects various physiological processes. Some studies have shown a connection between the dysregulation of iron levels and the development of different mental disorders, including schizophrenia. Abnormal levels of iron in a specific region of the brain have been observed in people with schizophrenia. Iron levels may contribute to the pathogenesis of schizophrenia in combination with other genetic, environmental and dietary factors. Iron can also contribute to the better cognitive functioning of a patient with schizophrenia, and due to frequent malnutrition and undernourishment in this group of patients, it is crucial to take into account the need for routine hematological examinations and the determination of essential nutritional deficiencies. Finally, our goals were to systematically review the literature published in the last two decades using PubMed, Web of Science, Scopus and Google Scholar. We described the clinical aspects and etiological factors of schizophrenia. We determined whether schizophrenia can be associated with iron concentration disorders to recognize and identify potential patients with iron deficiency and treat them promptly in daily clinical practice.

IntroductionClivus meningiomas are benign tumors that occur at the skull base in the posterior cranial fossa. Symptoms usually progress several months or years before diagnosis and may include: headache, vertigo, hearing impairment, ataxia with gait disturbances, sensory problems. In the neurological findings, paralysis of the lower cranial nerves is most often seen, which in the later course can be accompanied by cerebellar and pyramidal signs until the development of a consciousness impairment.Case presentationWe presented the case of a patient who at the time of diagnosis had only unilateral hypoglossal nerve paralysis with dysarthria and mild dysphagia. After the neurosurgical procedure, pathohistological analysis confirmed meningothelial meningioma.ConclusionEarly recognition of clivus tumors, which include meningiomas, is necessary in order to implement an adequate therapeutic procedure and prevent further deterioration of the patient’s condition.

Numerous studies on the health and functioning of veterans and former prisoners of war have shown that the experience of war captivity is one of the most difficult human experiences. Captivity is often characterized by extremely difficult and inhumane conditions, as well as exposure to various forms of both psychological and physical abuse. Such traumatic experiences can lead to serious psychological consequences that can last for years, even decades after release from captivity. The aim of this paper is to present a brief overview of research that points to the specifics of wartime captivity and the long-term psychological consequences in veterans of former camp detainees, as well as the consequences suffered by their families and factors that, apart from the intensity of the trauma, contribute to the emergence and persistence of psychological disorders. From the presented research, it can be concluded that former prisoners of the camp represent an extremely vulnerable group of the social community and require long-term appropriate treatment, while the needs of veterans’ families should not be neglected, with the necessity of including spouses and children in psychological and psychosocial treatments.