OGD-induced free radical production, a contributing factor in cell swelling, was significantly reduced by both myricetin and quercetin. However, depolarization of the inner mitochondrial membrane potential (Delta Psi(m)), the blockade of which generally reduces swelling, was significantly diminished by myricetin,

but not quercetin. This indicated that quercetin could reduce swelling despite its inability to prevent depolarization of Delta Psi(m) possibly through other signaling pathways. Increased intracellular calcium ([Ca(2+)](i)) is an important characteristic of ischemic selleck products injury and is implicated in swelling. Both myricetin and quercetin attenuated the increase in [Ca(2+)](i). Further, a reduction in [Ca(2+)](i), through the use of nifedipine, nimodipine, verapamil, dantrolene, or BAPTA-AM, significantly reduced www.selleckchem.com/products/sbe-b-cd.html OGD-induced cell swelling indicating that one possible mechanism by which such flavonoids attenuate cell swelling may be through regulating [Ca(2+)](i). OGD-induced decrease in glutamate uptake was attenuated by myricetin, but not quercetin. Cyclosporin A, a blocker of the mitochondrial permeability transition (mPT)

pore, but not FK506 (that does not block the mPT), attenuated the decline in glutamate uptake after OGD, indicating the involvement of the mPT in glutamate uptake. Our results indicated that while blockade of Delta Psi(m) may be sufficient to reduce swelling,

it may not be a necessary factor, and that flavonoids reduce cell swelling by regulating [Ca(2+)](i). The differential effects of myricetin and quercetin on OGD-induced reduction on glutamate uptake may be due to their differential Calpain effects on mitochondria. Published by Elsevier Ltd on behalf of IBRO.”
“It has been hypothesized that corticotropin-releasing factor (CRF) and its related neuropeptide urocortin 1 (Ucn1) play different roles in the initiation and adaptive phases of the stress response, which implies different temporal dynamics of these neuropeptides in response to stressors. We have tested the hypothesis that acute pain stress (APS) differentially changes the dynamics of CRF expression in the paraventricular nucleus of the hypothalamus (PVN), oval subdivision of the bed nucleus of the stria terminalis (BSTov) and central amygdala (CeA), and the dynamics of Ucn1 expression in the midbrain non-preganglionic Edinger Westphal nucleus (npEW). Thirty minutes after APS, induced by a formalin injection into the left hind paw, PVN, BSTov, CeA and npEW all showed a peak in cFos mRNA expression that was followed by a robust increase in cFos protein-immunoreactivity, indicating a rapid increase in (immediate early) gene expression in all four brain nuclei.