Glutathionylation of beta-actin via a cysteinyl sulfenic acid intermediary-5

<p><b>Copyright information:</b></p><p>Taken from "Glutathionylation of beta-actin via a cysteinyl sulfenic acid intermediary"</p><p>http://www.biomedcentral.com/1471-2091/8/26</p><p>BMC Biochemistry 2007;8():26-26.</p><p>Published online 10 Dec 2007</p><p>PMCID:PMC2228301.</p><p></p>he absence or presence of 1 mM diamide and 1 mM DTT. (B) Sensitivity of the assay for detection of glutathionylated actin coated on the plates

Glutathionylation of beta-actin via a cysteinyl sulfenic acid intermediary-4

<p><b>Copyright information:</b></p><p>Taken from "Glutathionylation of beta-actin via a cysteinyl sulfenic acid intermediary"</p><p>http://www.biomedcentral.com/1471-2091/8/26</p><p>BMC Biochemistry 2007;8():26-26.</p><p>Published online 10 Dec 2007</p><p>PMCID:PMC2228301.</p><p></p>del for glutathionylation of β-actin via a cysteinyl sulfenic acid intermediary (B)

Glutathionylation of beta-actin via a cysteinyl sulfenic acid intermediary-3

<p><b>Copyright information:</b></p><p>Taken from "Glutathionylation of beta-actin via a cysteinyl sulfenic acid intermediary"</p><p>http://www.biomedcentral.com/1471-2091/8/26</p><p>BMC Biochemistry 2007;8():26-26.</p><p>Published online 10 Dec 2007</p><p>PMCID:PMC2228301.</p><p></p>. Deglutathionylation of β-actin catalyzed by Grx1 (B

Glutathionylation of beta-actin via a cysteinyl sulfenic acid intermediary-1

<p><b>Copyright information:</b></p><p>Taken from "Glutathionylation of beta-actin via a cysteinyl sulfenic acid intermediary"</p><p>http://www.biomedcentral.com/1471-2091/8/26</p><p>BMC Biochemistry 2007;8():26-26.</p><p>Published online 10 Dec 2007</p><p>PMCID:PMC2228301.</p><p></p> indicated samples were incubated with (i) 1 mM DTT, after which 1 mM GSSG (A) or GSH (B) was added (ii) and a second incubation with 1 mM DTT was performed (iii)

Glutathionylation of beta-actin via a cysteinyl sulfenic acid intermediary-2

<p><b>Copyright information:</b></p><p>Taken from "Glutathionylation of beta-actin via a cysteinyl sulfenic acid intermediary"</p><p>http://www.biomedcentral.com/1471-2091/8/26</p><p>BMC Biochemistry 2007;8():26-26.</p><p>Published online 10 Dec 2007</p><p>PMCID:PMC2228301.</p><p></p>ted with actin as described in Methods, incubated first with 5 mM DTT to reduce thiols and then incubated with 1 mM GSH at 22°C. (B) Quantification of relative amounts of actin immobilized on the plates (primary amine groups labelled with NHS-biotin) and accessible free thiols (thiols labelled with NEM-biotin)

Ketamine decreases NSC viability in a dose-dependent manner.

<p>NSCs were plated as single cells treated with 50 μM, 200 μM, 400 μM and 1 mM ketamine. To measure cell viability, intracellular ATP levels were measured after 24 hours. Data are shown as mean ±SEM (n = 22–35). Kruskal-Wallis followed by Dunn’s test was used. Differences were considered significant at P <0.05. * denotes P<0.05 compared with control.</p

PACAP counteracts ketamine induced apoptosis and ER stress.

NSCs were plated as single cells and treated with 400 μM ketamine alone or with 100 nM PACAP and 400 μM ketamine. After 24 hours incubation, cells were harvested for Western blot analysis (A, B) or harvested for mRNA extraction and quantitative RT-PCR experiments (C). To obtain quantitative measurements Bcl-2 protein levels and cleaved caspase-3 were normalized against coomassie blue. Data are shown as mean ±SEM (A, n = 5–6; B, n = 3–5, C, n = 4–6). Kruskal-Wallis followed by Dunn’s test. Differences were considered significant at P<0.05. * denotes P<0.05 compared with control, # denotes P<0.05 compared to 400 μM ketamine.</p

MOESM1 of Somatic symptoms in adolescence as a predictor of severe mental illness in adulthood: a long-term community-based follow-up study

Additional file 1: Appendix S1. Frequencies of specific somatic symptoms and differences between individuals without and with adolescent depression. Appendix S2. Frequencies of any hospital-based mental health care diagnosis by specific somatic symptoms

PACAP Protects Adult Neural Stem Cells from the Neurotoxic Effect of Ketamine Associated with Decreased Apoptosis, ER Stress and mTOR Pathway Activation

<div><p>Ketamine administration is a well-established approach to mimic experimentally some aspects of schizophrenia. Adult neurogenesis dysregulation is associated with psychiatric disorders, including schizophrenia. The potential role of neurogenesis in the ketamine-induced phenotype is largely unknown. Recent results from human genetic studies have shown the pituitary adenylate cyclase-activating polypeptide (PACAP) gene is a risk factor for schizophrenia. Its potential role on the regulation of neurogenesis in experimental model of schizophrenia remains to be investigated. We aimed to determine whether ketamine affects the viability of adult neural stem cells (NSC). We also investigated whether the detrimental effect mediated by ketamine could be counteracted by PACAP. NSCs were isolated from the subventricular zone of the mouse and exposed to ketamine with/without PACAP. After 24 hours, cell viability, potential involvement of apoptosis, endoplasmic reticulum (ER) stress, mTOR and AMPA pathway activation were assessed by quantitative RT-PCR and Western blot analysis. We show that ketamine impairs NSC viability in correlation with increased apoptosis, ER stress and mTOR activation. The results also suggest that the effect of ketamine occurs <i>via</i> AMPA receptor activation. Finally, we show that PACAP counteracted the decreased NSC viability induced by ketamine <i>via</i> the specific activation of the PAC-1 receptor subtype. Our study shows that the NSC viability may be negatively affected by ketamine with putative importance for the development of a schizophrenia phenotype in the ketamine induced animal model of schizophrenia. The neuroprotective effect via PAC-1 activation suggests a potentially novel pharmacological target for the treatment of schizophrenia, <i>via</i> neurogenesis normalization.</p></div

Ketamine-induced cell death is counteracted by PACAP <i>via</i> PAC-1 receptor activation.

<p>NSCs were plated as single cells. Cells were incubated with 400 μM ketamine and PACAP (100 nM) or agonist for PAC-1; Max-4 (30 nM). After 24 hour incubation, intracellular ATP levels were measured for cell viability. Data are shown as mean ±SEM (n = 13–39). Kruskal-Wallis followed by Dunn’s test was used. Differences were considered significant at P<0.05. * denotes P<0.05 compared with control, # denotes P<0.05 compared to 400 μM ketamine.</p