Neuropsychobiology

The chronic mild stress (CMS) model of depression has high validity but has in the past been criticized for being difficult to replicate. However, a large number of recent publications have confirmed that CMS causes behavioural changes in rodents that parallel symptoms of depression. This review summarizes studies from over sixty independent research groups that have reported decreases in reactivity to rewards, and a variety of other depression-like behaviours, in rats or mice, following exposure to CMS. Together, these changes are referred to as a ‘depressive’ behavioural profile. Almost every study that has examined the effects of chronic antidepressant treatment in these procedures has reported that antidepressants were effective in reversing or preventing these ‘depressive’ behavioural changes. (The single exception is a study in which the duration of treatment was too brief to constitute an adequate trial.) There are also a handful of reports of CMS causing significant effects in the opposite direction, termed here an ‘anomalous’ behavioural profile. There are six neurobiological parameters that have been studied in both ‘anhedonic’ and ‘anomalous’ animals: psychostimulant and place-conditioning effects of dopamine agonists; dopamine D₂ receptor number and message; inhibition of dopamine turnover by quinpirole, and beta-adrenergic receptor binding. On all six measures, CMS caused opposite effects in animals displaying ‘depressive’ and ‘anomalous’ profiles. Thus, there is overwhelming evidence that under appropriate experimental conditions, CMS can cause antidepressant-reversible depressive-like effects in rodents; however, the ‘anomalous’ profile that is occasionally reported appears to be a genuine phenomenon, and these two sets of behavioural effects appear to be associated with opposite patterns of neurobiological changes.

There is increasing evidence for an association between the alteration of cytokine concentrations in blood and the pathophysiology of depressive disorders. Studies in humans have not investigated CSF cytokine concentrations and their relationship to depressive disorders. This study reports on the association of the CSF concentration of proinflammatory cytokines, IL-1β, IL-6 and TNFα, and major depressive disorders. CSF samples were obtained from 13 hospitalized patients with acute unmedicated severe depression and were compared with 10 control subjects. Compared to the control group, the depressed patient group had higher CSF concentrations of IL-1β, lower IL-6 and no change in TNFα. A positive correlation was found between serum IL-1β and the severity of depression. These results indicate a unique profile for CSF proinflammatory cytokines in acute depression. These findings merit further investigation and if replicated may possibly offer immunological treatment options for depression.

We had previously reported decreased serum brain-derived neurotrophic factor (BDNF) levels in depressed patients. In the present study, we tested the hypothesis that antidepressant treatment would normalize serum BDNF levels, at least in a subgroup of patients. Major depressed patients (15 females and 11 males) diagnosed according to DSM-IV criteria and healthy controls (13 females and 13 males) participated in this study. Serum BDNF was assayed with the ELISA method for depressed and remitted patients and the severity of depression was evaluated with the Montgomery-Asberg Depression Rating Scale. An analysis of variance showed that treatment had an effect [F(1, 24) = 4.46, p = 0.045] on the normalization of serum BDNF levels. We also found a correlation between the severity of depression (r = 0.51, p = 0.008), the pretreatment BDNF levels (r = 0.62, p = 0.001) and the difference in serum BDNF levels after antidepressant treatment. These results suggest that antidepressant treatment has a positive effect on serum BDNF levels and support the hypothesis of neurotrophic factor involvement in affective disorders.

The etiopathogenesis of eating disorders (ED) is complex and poorly understood. Biological, psychological and environmental factors have all been considered to be involved in the onset and the persistence of these syndromes, often with conflicting results. The recent literature focused on the possible role of hormonal pathways, in particular the hypothalamic-pituitary-adrenal (HPA) axis, as a relevant factor capable of influencing the onset and the course of ED. Other studies have suggested that the onset of ED is often preceded by severe life events, and that chronic stress is associated with the persistence of these disorders. As the biological response to stress is the activation of the HPA axis, the available literature considering the relationships between stress, HPA axis functioning and anorexia nervosa, bulimia nervosa and binge eating disorder is reviewed by the present article.

Meditation is a specific consciousness state in which deep relaxation and increased internalized attention coexist. There have been various neurophysiological studies on meditation. However, the personal predispositions/traits that characterize the properties of meditation have not been adequately studied. We analyzed changes in neurophysiological parameters [EEG coherence and autonomic nervous activity using heart rate variability (HRV) as an index] during Zen meditation, and evaluated the results in association with trait anxiety (assessed by Spielberger’s State-Trait Anxiety Inventory) in 22 healthy adults who had not previously practiced any form of meditation. During meditation, in terms of mean values in all subjects, an increase in slow alpha interhemispheric EEG coherence in the frontal region, an increase in high-frequency (HF) power (as a parasympathetic index of HRV), and a decrease in the ratio of low-frequency to HF power (as a sympathetic index of HRV) were observed. Further evaluation of these changes in individuals showed a negative correlation between the percent change (with the control condition as the baseline) in slow alpha interhemispheric coherence reflecting internalized attention and the percent change in HF reflecting relaxation. The trait anxiety score was negatively correlated with the percent change in slow alpha interhemispheric coherence in the frontal region and was positively correlated with the percent change in HF. These results suggest that lower trait anxiety more readily induces meditation with a predominance of internalized attention, while higher trait anxiety more readily induces meditation with a predominance of relaxation.

Several studies have underlined the high prevalence of psychiatric symptoms and disorders in thyroid diseases. The aim of this study was to evaluate the prevalence of psychiatric disorders in 93 inpatients affected by different thyroid diseases during their lifetimes, by means of a standardized instrument, i.e., the Structured Clinical Interview for Diagnostic and Statistical Manual of Mental Disorders-III-Revised, Upjohn Version (SCID-UP-R). The results showed higher rates of panic disorder, simple phobia, obsessive-compulsive disorder, major depressive disorder, bipolar disorder and cyclothymia in thyroid patients than in the general population. These findings would suggest that the co-occurrence of psychiatric and thyroid diseases may be the result of common biochemical abnormalities.