Lucifer yellow propagation was inhibited by gap junction blockers. Our findings show that the glial syncitium propagates SPM through gap junctions and further indicate a new role of polyamines in the regulation of the astroglial network under both normal and pathological conditions. NeuroReport 23:1021-1025 (C) 2012 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.”
“In this study, we

evaluated the involvement of N-methyl-d-aspartate receptor (NMDAR)/nitric oxide (NO) system on the antidepressant-like effects of Prexasertib cost paroxetine in the mouse forced swimming test.

Swim sessions were conducted by placing mice in individual glass cylinders filled with water for 6 min. The duration of behavioral immobility during the last 4 min of the test was evaluated.

Paroxetine (8 and 16 mg/kg, intraperitoneal [i.p.]) significantly reduced the immobility times of mice, whereas lower doses (2 and 4 mg/kg) had no effect. NMDA antagonists MK-801 (0.1 and 0.25 mg/kg, i.p.) and ifenprodil

(1 and 3 mg/kg, i.p.) and the NO synthase inhibitor N(G)-l-arginine methyl ester (L-NAME; 30 and 100 mg/kg, i.p.) significantly decreased Temsirolimus purchase the immobility time. Lower doses of MK-801 (0.01 and 0.05 mg/kg), ifenprodil (0.1 and 0.5 mg/kg), and L-NAME (10 mg/kg) had no effect. Combined treatment of subeffective doses of paroxetine (4 mg/kg) and MK-801 (0.05 mg/kg), ifenprodil (0.5 mg/kg), and L-NAME (10 mg/kg) robustly exerted an antidepressant-like effect. The noneffective dose of a NO precursor l-arginine

(750 mg/kg, i.p.) prevented the antidepressant-like effect of paroxetine (30 mg/kg).

We suggested, for the first time, a possible role for NMDAR/NO signaling in the antidepressant-like effects of paroxetine, providing a new approach for the treatment of depression.”
“The auditory-evoked potential’s N1 component of the scalp electroencephalogram is a well-established measure of electrical brain activity. The N1 reflects basic auditory processing and is modulated by auditory experience, for instance, by musical training. Here, we explore a possible correlation between the auditory N1 amplitude and cortical architecture in the supratemporal plane. We hypothesize that individual differences in N1 amplitude reflect differential acuity, which might also be reflected by Sotrastaurin differences in auditory cortex anatomy. Auditory potentials evoked by sine wave tones and structural MRI were collected from 27 healthy volunteers. The thickness and surface area of the cortex were calculated using a surface-based morphometry approach. Cortical thickness, rather than surface area, in a cluster on the posterior supratemporal plane, predominantly located on Heschl’s sulcus and lateral aspects of Heschl’s gyrus, correlated with the N1 amplitude. In particular, lower cortical thickness was associated with larger N1 amplitudes.