Dry Eye Syndrome, Posttraumatic Stress Disorder, and Depression in an Older Male Veteran Population.

Dry Eye Syndrome, Posttraumatic Stress Disorder, and Depression in an Older Male Veteran Population.

Invest Ophthalmol Vis Sci. 2013 Apr 30;
Fernandez CA, Galor A, Arheart KL, Musselman DL, Venincasa VD, Florez HJ, Lee DJ

PURPOSE: To evaluate whether veterans with posttraumatic stress disorder (PTSD) or depression have differences in dry eye symptoms and signs compared to a population without these conditions. METHODS: Male patients aged ?50 years with normal eyelid, conjunctival, and corneal anatomy were recruited from the Miami Veterans Affairs eye clinic (N=248). We compared dry eye symptoms (determined by the Dry Eye Questionnaire 5 [DEQ5] score) to tear film indicators obtained by clinical examination (i.e., tear osmolarity, corneal staining, tear breakup time, Schirmer’s, meibomian gland quality, orifice plugging, lid vascularity), between patients with PTSD or depression versus those without these conditions. Student T-tests, Chi-squared analyses, and linear and logistic regressions were used to assess differences between the groups. RESULTS: DEQ5 scores were higher in the PTSD (mean=13.4; standard error[SE]=1.1; n=22) and depression (mean=12.0; SE=0.8; n=40) groups compared to the group without these conditions (mean=9.8; SE=0.4; n=186; p<0.01 and p=0.02, respectively). More patients in the PTSD and depression groups had severe dry eye symptoms, defined as a DEQ5 score of ?12 (77% and 63% vs. 41%; p<0.01 and p=0.02, respectively). No significant differences in tear film indicators were found among the three groups. Multivariable logistic regression indicated that a PTSD diagnosis (OR=4.08; 95%CI=1.10-15.14) and use of selective serotonin reuptake inhibitors (OR=2.66; 95%CI=1.01-7.00) were significantly associated with severe symptoms. CONCLUSION: Patients with PTSD have ocular surface symptoms that are not solely explained by tear indicators. Identifying underlying conditions associated with ocular discomfort is essential to better understand the mechanisms behind ocular pain in DES. HubMed – depression


Fast neurotransmitter release regulated by the endocytic scaffold intersectin.

Proc Natl Acad Sci U S A. 2013 Apr 30;
Sakaba T, Kononenko NL, Bacetic J, Pechstein A, Schmoranzer J, Yao L, Barth H, Shupliakov O, Kobler O, Aktories K, Haucke V

Sustained fast neurotransmission requires the rapid replenishment of release-ready synaptic vesicles (SVs) at presynaptic active zones. Although the machineries for exocytic fusion and for subsequent endocytic membrane retrieval have been well characterized, little is known about the mechanisms underlying the rapid recruitment of SVs to release sites. Here we show that the Down syndrome-associated endocytic scaffold protein intersectin 1 is a crucial factor for the recruitment of release-ready SVs. Genetic deletion of intersectin 1 expression or acute interference with intersectin function inhibited the replenishment of release-ready vesicles, resulting in short-term depression, without significantly affecting the rate of endocytic membrane retrieval. Acute perturbation experiments suggest that intersectin-mediated vesicle replenishment involves the association of intersectin with the fissioning enzyme dynamin and with the actin regulatory GTPase CDC42. Our data indicate a role for the endocytic scaffold intersectin in fast neurotransmitter release, which may be of prime importance for information processing in the brain. HubMed – depression


Prior history of chronic stress changes the transcriptional response to glucocorticoid challenge in the dentate gyrus region of the male rat hippocampus.

Endocrinology. 2013 Apr 30;
Datson NA, van den Oever JM, Korobko OB, Magarinos AM, de Kloet ER, McEwen B

Chronic stress is a risk factor for several neuropsychiatric diseases such as depression and psychosis. In response to stress glucocorticoids (GCs) are secreted that bind to the glucocorticoid receptor (GR), a ligand-activated transcription factor that regulates the transcription of gene networks in the brain necessary for coping with stress, recovery and adaptation. Chronic stress particularly affects the dentate gyrus (DG) subregion of the hippocampus, causing several functional and morphological changes with consequences for learning and memory, that are likely adaptive, but at the same time make DG neurons more vulnerable to subsequent challenges.The aim of this study was to investigate the transcriptional response of DG neurons to a GC-challenge in male rats previously exposed to chronic restraint stress (CRS). An intriguing finding of the current study was that having a history of CRS had profound consequences for the subsequent response to acute GC-challenge, differentially affecting the expression of several hundreds of genes in the DG compared to challenged non-stressed control animals. This enduring effect of prior stress exposure suggests that epigenetic processes may be involved. In line with this, CRS indeed affected the expression of several genes involved in chromatin structure and epigenetic processes, including Asf1, Ash1l, Hist1h3f and Tp63. The data presented here indicate that CRS alters the transcriptional response to a subsequent GC-injection. We propose that this altered transcriptional potential forms part of the molecular mechanism underlying the enhanced vulnerability for stress-related disorders like depression caused by chronic stress. HubMed – depression