Different effect of serotonin on intracellular calcium ion dynamics in the smooth muscle cells between rat posterior ciliary artery and vorticose vein.

5-hydroxytriptamine (5-HT: serotonin) is an important transmitter that causes vessel constriction, although few studies have examined the effect of 5-HT on venous smooth muscles. The intracellular Ca(2+) concentration ([Ca(2+)]i) plays an essential role in stimulus-response coupling in numerous tissue/cells including vascular smooth muscle cells. The present study was performed to examine whether differences between arteries and veins in the response to 5-HT can be detected under confocal microscope with respect to [Ca(2+)]i dynamics. In posterior ciliary arteries of rats, 5-HT induced a [Ca(2+)]i increase. The 5-HT-induced responses were caused by both Ca(2+) influx and mobilization. Agonist and antagonist experiments revealed that arterial smooth muscles possess 5-HT1a, 1b, 2 (Gprotein-coupled type) and 5-HT3 (ion channel type) receptors, and that 5-HT2 in particular plays a major role in these responses. For vorticose veins, the 5-HT-induced responses were also caused by both Ca(2+) influx and mobilization. However, the cAMP dependent pathway (5-HT4-7) was found to be significant in vasocontraction with respect to 5-HT in these vessels. Thus, Ca(2+) mobilization was induced by 5-HT2 and 5-HT4-7 in a vessel-dependent manner, whereas Ca(2+) influx universally was induced by 5-HT3. These results indicate that the posterior ciliary arteries and vorticose veins in the same tissue might differ greatly in their responses to stimulus.

Proton magnetic resonance spectroscopy and diffusion-weighted imaging of tumefactive demyelinating plaque.

Proton magnetic resonance spectroscopy, diffusion-weighted axonography, and diffusion tensor tractography in a patient with tumefactive demyelination plaque (TDP) were evaluated for differential diagnosis from glioblastoma. The findings of glutamate and glutamine elevations on magnetic resonance spectroscopy and apparent tracts within the lesion on axonography and tractography were unlikely to represent glioblastoma, and were thus useful for the preoperative diagnosis of TDP.

Microtubule remodeling mediates the inhibition of store-operated calcium entry (SOCE) during mitosis in COS-7 cells.

Regulation of the intracellular calcium ion concentration ([Ca(2+)](i)) is critical, because calcium signaling controls diverse and vital cellular processes such as secretion, proliferation, division, gene transcription, and apoptosis. Store-operated calcium entry (SOCE) is the main mechanism through which non-excitable cells replenish and thus maintain this delicate balance. There is limited evidence which indicates that SOCE may be inhibited during mitosis, and the mechanisms leading to the presumed inhibition has not been elucidated. In the present study, we examined and compared the [Ca(2+)](i) dynamics of COS-7 cells in mitotic and non-mitotic phases with special reference paid to SOCE. Laser scanning confocal microscopy to monitor [Ca(2+)](i) dynamics revealed that SOCE was progressively inhibited in mitosis and became virtually absent during the metaphase. We used various cytoskeletal modifying drugs and immunofluorescence to assess the contribution of microtubule and actin filaments in SOCE signaling. Nocodazole treatment caused microtubule reorganization and retraction from the cell periphery that mimicked the natural mitotic microtubule remodeling that was also accompanied by SOCE inhibition. Short exposure to paclitaxel, a microtubule-stabilizing drug, bolstered SOCE, whereas long exposure resulted in microtubule disruption and SOCE inhibition. Actin-modifying drugs did not affect SOCE. These findings indicate that mitotic microtubule remodeling plays a significant role in the inhibition of SOCE during mitosis.

Immunohistochemical localization of protease-activated receptors in cerebral and testicular arterioles of rats: their dependence on arteriole size and organ-specificity.

Protease-activated receptors (PARs) expressed in the endothelia and smooth muscles of vessels may play important roles in blood vessel function. Using intracellular calcium ion concentration ([Ca2+]i) imaging, we recently observed that small - but not large - arterioles of the brain responded to proteases, while testicular arterioles showed no response. The purpose of the present study was to examine the heterogeneity of the localization of PARs in arterioles using immunohistochemistry. Consistent with the [Ca2+]i imaging results, neither the thrombin receptor nor PAR2 were evident in large arterioles of the brain. However, the small arterioles of the brain, vascular smooth muscles, and endothelia showed a distinct immunoreactivity against the thrombin receptor and PAR2. The immunoreactivity of PARs in testicular arterioles was faint. In conclusion, size-dependent and/or organ-specific responses of arterioles to proteases are due to the heterogeneous localization of PARs.

Regional differences in 5-HT receptors in cerebral and testicular arterioles of the rat as revealed by Ca2+ imaging of real-time confocal microscopy: variances by artery size and organ specificity.

5-hydroxytriptamine (5-HT) is an important transmitter for vessel constriction. The present study was performed to clarify the effect of 5-HT on smooth muscles in large- and small-sized cerebral and testicular arterioles by confocal microscopy, with special reference to intracellular Ca2+ concentration ([Ca2+]i) dynamics. In cerebral vessels, 5-HT induced a [Ca2+]i increase and the contraction of smooth muscle cells in large- and midsized arterioles (external diameters>50 microm) but not in small-sized arterioles. Conspicuous [Ca2+]i changes by 5-HT were especially observed in the portions close to the cerebral arterial circle, and the 5-HT-induced responses were caused by both Ca2+ influx and mobilization. Experiments using agonists and antagonists also revealed that cerebral arteriole smooth muscles possess 5-HT1a, 1b, 2 (G-protein-coupled type), and 3 (ion channel type) receptors; specifically, 5-HT2 plays a major role in these responses. On the other hand, in testicular vessels, there were few regional differences among responses to 5-HT, and both large- and small-sized arterioles responded to 5-HT. The responses were caused by only Ca2+ mobilization mediated 5-HT1a and 2. These results indicate that arterioles in different tissues may respond to 5-HT in different manners. Regional differences and the size-dependent manner of responses to 5-HT in cerebral blood vessels also indicate that the regulatory mechanism of blood circulation is highly differentiated in each region of the central nervous system.