IL-2 levels in the brain were analyzed by enzyme-linked immunoadsorbent assays. Inescapable and escapable stressors had different effects on behavior in the modified active avoidance test and on IL-2 levels in brain areas that are known to be involved in emotional processes. These

data provide insight into the pathophysiological role of IL-2 in stress-related disorders.”
“Herein, we show that a single injection of P4 (4 mg/kg) at 1 h or 48 h, but not 96 h, before middle cerebral artery occlusion (MCAO) produces significant MI-503 nmr protective effects against the ischemia-induced neuronal death and the deficits in spatial cognition and UP induction. The present study focused on the molecular mechanisms underlying the neuroprotection exerted by P4 administration

at I h and 48 h pre-MCAO, termed acute and delayed P4-neuroprotection, respectively. Pharmacology suggested that P4-receptor (P4R) cascading to a Src-ERK1/2 signaling mediated the delayed P4-neuroprotection. To support this, it was observed by anti-phosph-ERK1/2 immunoblots that a single injection of P4 triggered a P4R-mediated https://www.selleckchem.com/products/q-vd-oph.html persistent increase in ERK1/2 phosphorylation and their nuclear translocation for 48 h. In contrast, the acute P4-neuroprotection did not depend on the P4R-mediated Src-ERK1/2 signaling. Instead, the acute P4-administration attenuated the NMDA-induced rise in the intracellular calcium concentration ([Ca(2+)](i)) that may be a primary cause for MCAO-induced neuronal injury. This effect seemed Rutecarpine to be exerted by an antagonism of sigma(1) receptor since the sigma(1) receptor antagonist NE100 perfectly mimicked the acute P4-neuroprotection and also attenuated the NMDA-induced [Ca(2+)](i), increase. These findings suggest that the P4 neuroprotection

involves two independent processes depending on the timing of P4 administration before MCAO: an acute protection by antagonizing sigma(1) receptor to inhibit NMDAr-Ca(2+) influx and a delayed one by an activation of P4R-mediated Src-ERK signaling pathway. (C) 2008 Elsevier Ltd. All rights reserved.”
“Effects of the gap junction blocker carbenoxolone (CBX) on tetanus- and taurine-induced long-term potentiation (LTP) were studied on Schaffer collateral-CA1 field excitatory postsynaptic potentials (fEPSPs) in mouse hippocampal slices. Preincubation with 10 mu M CBX reduced the amount of LTP induced by weak theta-burst stimulation (TBS) or a single train of stimuli (HFS; 1 s at 100 Hz), but did not affect LTP induced by 30-min perfusion with 10 mM taurine. Incubation with 50-100 mu M CBX 15 min before HFS or TBS abolished tetanus-induced LTP. At 100 mu M CBX, the concentration that is used for the blockade of gap junctions in vitro, a long-lasting depression of fEPSPs was observed which persisted under the blockade of NMDA receptors, and receptors for corticosteroids.