Neuroscience
-
The sphenopalatine ganglion (SPG) is a gathering of the cell bodies of parasympathetic fibers that dominate the nasal gland, lacrimal gland and cerebral blood vessels. The SPG controls nasal secretions, tears, and the dilation of cerebral blood vessels. However, it is unclear how serotonin regulates SPG functions. ⋯ The 5-HT3A receptor, 5-HT3B receptor, and AADC were expressed in 96.5% ± 1.0%, 29.7% ± 10.7%, and 57.4% ± 2.9% of neuronal cell bodies in the SPG, respectively, indicating that the 5-HT3A receptor was virtually expressed in all SPG neurons. Our results on the expression of these critical serotonin system genes in the parasympathetic SPG provide insight into the pathogenetics of rhinitis, conjunctivitis and headache. Furthermore, our findings suggest that targeting the 5-HT3A receptor might have therapeutic potential in the treatment of these ailments.
-
Individuals continuously confronted with various stresses in modern life generate high levels of cortisol (corticosterone in rodents), the major glucocorticoid secreted by adrenal gland when hypothalamic-pituitary-adrenal axis is activated. Chronic stress can induce constant release of glucocorticoid and cause many serious health problems, such as mental disorders, cardiovascular diseases and autoimmune diseases. Many studies have suggested the neurotoxic effect of corticosterone is mediated through increased oxidative stress and apoptosis. ⋯ By utilizing a cellular stress model of exposing cells to corticosterone, our study found that there were a dose-dependent decrease in SIRT1 and an increase in LC3B II/I expressions with increasing concentrations of corticosterone. In combination with SIRT1 overexpression and knockdown plasmids, the regulation of SIRT1 expression in vitro demonstrated that SIRT can inhibit corticosterone-induced autophagy and enhance cell apoptosis. These findings might help us better understand the role of SIRT1 and autophagy activation in chronic stress.
-
In hypertensive retinopathy, the retinal damage due to high blood pressure is accompanied by increased expression of Glial Fibrillary Acidic Protein (GFAP), which indicates a role of neuroinflammatory processes in such a retinopathy. Proteins belonging to the Rho GTPase family, particularly Rac1, are involved in the activation of Müller glia and in the progression of photoreceptor degeneration, and may thus represent a novel candidate for therapeutic intervention following central nervous system inflammation. ⋯ Furthermore, such functional improvement is accompanied by a reduction of Rac1 activity and retinal GFAP expression. Our results suggest that Rac1 inhibition through CNF1 topical administration may represent a new strategy to target retinal gliosis.
-
Neurobrucellosis, which is the most morbid form of brucellosis disease, presents with inflammatory signs and symptoms. Recent experimental evidence clearly indicates that deregulation of astrocytes and microglia caused by Brucella infection creates a microenvironment in the central nervous system (CNS) in which secretion of pro-inflammatory mediators lead to destabilization of the glial structure, the damage of the blood brain barrier (BBB) and neuronal demise. This review of Brucella interactions with cells of the CNS and the BBB is intended to present recent immunological findings that can explain, at least in part, the basis for the inflammatory pathogenesis of the nervous system that takes place upon Brucella infection.