An MRI time course of 512 echo-planar images (EPI) in resting human brain obtained every 250 ms reveals fluctuations in signal intensity in each pixel that have a physiologic origin. Regions of the sensorimotor cortex that were activated secondary to hand movement were identified using functional MRI methodology (FMRI). Time courses of low frequency (< 0.1 Hz) fluctuations in resting brain were observed to have a high degree of temporal correlation (P < 10(-3)) within these regions and also with time courses in several other regions that can be associated with motor function. It is concluded that correlation of low frequency fluctuations, which may arise from fluctuations in blood oxygenation or flow, is a manifestation of functional connectivity of the brain.

Functional connectivity in the motor cortex of resting human brain using echo-planar MRI.

Background: Childhood abuse has been associated with negative adult health outcomes, including obesity. This study sought to investigate the association between c

/pdf/carrying-the-pain-of-abuse-gender-specific-findings-on-the-4hxvl3d9b4.pdf

Carrying the Pain of Abuse: Gender-Specific Findings on the Relationship between Childhood Physical Abuse and Obesity in Adulthood

Depression is a multicausal disorder and has been associated with the risk to develop cancer, dementia, diabetes, epilepsy and stroke. As a metabolic disorder depression has been associated with obesity, diabetes, insulin sensitivity, neuropeptide Y, glucose regulation, poor glycemic control, glucagone-like peptide-1, cholezystokinin, ghrelin, leptin, the endocannabinoid system, insulin-like growth factor and gastrin-releasing peptide. As a cardiovascular disease a close relationship exists between depression and blood pressure, heart rate, norepinephrine, sympathetic tone, vascular resistance, blood viscosity, plasma volume, intima thickness and atherosclerosis. Additionally blood coagulation, fibrinolysis, D-dimers, plasminogen activator inhibitor-1 protein, platelet activation, VEGF, plasma nitric oxide and its synthase are changed in depressed patients. As an endocrinological and stress disorder depression has been connected with the concentration of free T4, TSH, CRH, arginine vasopressin, corticotrophin, corticosteroid release and ACTH. Depression as an inflammatory disorder is mediated by pro-inflammatory cytokines, interleukin-1, interleukin-6, TNF-alpha, soluble interleukin-2 receptors, interferon-alpha, interleukin 8, interleukin-10, hs-CRP, acute phase proteins, haptoglobin, toll like receptor 4, interleukin-1beta, mammalian target of rapamycin pathway, substance P, cyclooxygenase-2, prostaglandin-E2, lipid peroxidation levels and acid sphingomyelinase. Nutritional factors might influence depression risk, i.e. the consumption of folate, omega-3 fatty acids, monounsaturated fatty acids, olive oil, fish, fruits, vegetables, nuts, legumes, vitamin B6 and vitamin B12. The neurodegenerative hypothesis of depression explains decreased hippocampal volumes in depressed patients and changes of neurotrophic support by BDNF, erythropoietin, GDNF, FGF-2, NT3, NGF and growth hormone. In this context, a fast neuroprotective and antidepressant effect has also been observed by ketamine, which acts via the glutamatergic system. Hence, GABA, AMPA, EAAT, NMDA- and metabotropic glutamate receptors (mGluR1 to mGluR8) have gained interest in depression recently. Alternative, causative or also easy available treatment strategies beyond serotonin and noradrenaline reuptake inhibition might be a major topic of future psychiatric care. In this review, an attempt is made to overview concepts of the disease and search for perspectives on antidepressant treatment strategies beyond approved medications.

/pdf/molecular-mechanisms-of-depression-perspectives-on-new-51kg9254ke.pdf

Molecular Mechanisms of Depression: Perspectives on New Treatment Strategies

The secretion of glucocorticoids (GCs) is a classic endocrine response to stress. Despite that, it remains controversial as to what purpose GCs serve at such times. One view, stretching back to the time of Hans Selye, posits that GCs help mediate the ongoing or pending stress response, either via basal levels of GCs permitting other facets of the stress response to emerge efficaciously, and/or by stress levels of GCs actively stimulating the stress response. In contrast, a revisionist viewpoint posits that GCs suppress the stress response, preventing it from being pathologically overactivated. In this review, we consider recent findings regarding GC action and, based on them, generate criteria for determining whether a particular GC action permits, stimulates, or suppresses an ongoing stressresponse or, as an additional category, is preparative for a subsequent stressor. We apply these GC actions to the realms of cardiovascular function, fluid volume and hemorrhage, immunity and inflammation, metabolism, neurobiology, and reproductive physiology. We find that GC actions fall into markedly different categories, depending on the physiological endpoint in question, with evidence for mediating effects in some cases, and suppressive or preparative in others. We then attempt to assimilate these heterogeneous GC actions into a physiological whole. (Endocrine Reviews 21: 55‐ 89, 2000)

/pdf/how-do-glucocorticoids-influence-stress-responses-4egr3fa2k0.pdf

How do glucocorticoids influence stress responses? Integrating permissive, suppressive, stimulatory, and preparative actions.

In response to a peripheral infection, innate immune cells produce pro-inflammatory cytokines that act on the brain to cause sickness behaviour. When activation of the peripheral immune system continues unabated, such as during systemic infections, cancer or autoimmune diseases, the ensuing immune signalling to the brain can lead to an exacerbation of sickness and the development of symptoms of depression in vulnerable individuals. These phenomena might account for the increased prevalence of clinical depression in physically ill people. Inflammation is therefore an important biological event that might increase the risk of major depressive episodes, much like the more traditional psychosocial factors.

/pdf/from-inflammation-to-sickness-and-depression-when-the-immune-maw2hn72o8.pdf

From inflammation to sickness and depression: when the immune system subjugates the brain

Efficacy and Safety of Xanomeline, a M1/M4 Receptor Preferencing Agonist, Plus Trospium, a Peripheral Muscarinic Antagonist, in Schizophrenia: Phase 2 Clinical Trial Results

Biology of Depression and Cytokines in Cancer

Neuroendocrine-Immune Interactions

P.1.155 Steroid-independent translocation of the glucocorticoid receptor by the antidepressant, desipramine

This study examined the ability of three replacement doses of corticosterone, aldosterone, or RU28362 to prevent the increase in morning basal plasma ACTH levels that occurs after adrenalectomy. In addition, the effect of each of these systemic steroid treatments on available cytosolic type I and type II corticosteroid receptor binding levels in hypothalamus, pituitary and hippocampus was measured. Available corticosteroid receptor measures indicated that the low dose of corticosterone occupied type I receptors, whereas the middle and high doses of corticosterone occupied both type I and type II receptors. Each of the doses of RU28362 selectively occupied type II receptors, whereas each of the doses of aldosterone selectively occupied type I receptors. The lowest dose of corticosterone partially prevented, and the middle and high doses of corticosterone completely prevented the adrenalectomy-induced increase in ACTH. Each of the doses of RU28362 prevented the adrenalectomy-induced increase in ACTH, whereas none of the doses of aldosterone had an effect on ACTH levels. These results substantiate the in vivo corticosteroid receptor subtype selectivity of aldosterone and RU28362. In addition, these results indicate that corticosteroid activation of neural type II receptors is sufficient to maintain morning levels of basal ACTH secretion. Type I corticosteroid receptor activation in the brain may also be sufficient to maintain basal ACTH levels, but only in response to corticosterone, not in response to aldosterone.

Maintenance of Basal ACTH Levels by Corticosterone and RU28362, but not Aldosterone: Relationship to Available Type I and Type II Corticosteroid Receptor Levels in Brain and Pituitary

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