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Mariko Taniai

Publications and source records attributed to Mariko Taniai.

4 recordsLinked to original sources
PubMed2003

Effect of MCI-9042, a 5-HT2 receptor antagonist, on retinal ganglion cell death and retinal ischemia.

The neuroprotective effect of MCI-9042 (Mitsubishi Pharma Corporation) was investigated on glutamate-induced retinal ganglion cell (RGC) death in vitro and on rat retinal ischemia in vivo. RGCs were purified from retinal cells isolated from 6-day-old Wistar rats and cultured in serum-free media. After application of 25 microM glutamate, the viability of RGCs treated with or without several serotonin 2 (5-HT(2)) receptor antagonists: MCI-9042, M-1 (a major metabolite of MCI-9042), ketanserin, and LY-53857; was evaluated by calcein-acetoxymethyl ester staining. Retinal ischemia was induced by intraocular pressure (IOP) elevation (130 mmHg, 50 min). Rats were intraperitoneally injected with MCI-9042 at a dose of 3, 30 mg/kg or base at 30 min before and just after ischemia-reperfusion. Retinal damages were evaluated by histology, morphometric analysis and electroretinograms (ERGs) recordings at 7 days after ischemia-reperfusion. 25 microM glutamate decreased the number of viable RGCs to about 60 to 65% of untreated RGCs. MCI-9042, M-1, ketanserin, and LY-53857 significantly reduced glutamate-induced RGC death at concentrations of more than 100 nM, 1 nM, 1 microM and 100 nM, respectively. Ischemia-reperfusion caused thinning of the thickness between the inner plexiform layer and the outer plexiform layer and attenuation of a-and b-waves in ERG recordings. The intraperitoneal injection of MCI-9042 significantly reduced morphological and functional damages in retinal ischemia. Our data demonstrate that 5-HT(2) receptor antagonists including MCI-9042 and M-1 have the neuroprotective effects in cultured RGCs and that MCI-9042 protects against ischemic retinal diseases.

Animals↗
PubMed2002

Binocular interaction reflected in visually evoked cortical potentials as studied with pseudorandom stimuli.

PURPOSE: To study the interaction of visual signals from both eyes with visual evoked cortical potentials (VECPs) elicited by pseudorandom binary sequence (PRBS) stimuli. METHODS: A PRBS was used to drive two independent LED arrays to elicit VECPs. The right and left eyes were simultaneously stimulated by two different series of PRBS stimuli. The impulse response function of each eye was calculated from the raw data by cross-correlating the PRBS and the response. The effect of changing the luminosity of the LEDs parametrically on the responses obtained from the two eyes was evaluated. RESULTS: The impulse response, obtained from 10 volunteers with normal vision, had characteristics similar to responses to the conventional VECP, with a major positive peak at 110 ms (P110). When two eyes were bilaterally exposed to two PRBS stimuli of the same luminosity, the P110 amplitudes of both eyes were decreased by the same amount from that obtained by stimulating only one eye. When the luminosity in the two eyes was different, the VECP amplitude in the eye with the dimmer stimuli decreased, and the amplitude in the contralateral eye increased. CONCLUSIONS: The results clearly demonstrate that interocular luminance interaction can be detected electrophysiologically in normal subjects by using PRBS- driven stimuli in which the feasibility of recording response from the two eyes independently.

Adult↗
PubMedDate not supplied

Protective action of nipradilol against ischemia-induced retinal damage in rats.

The purpose of this study was to investigate whether nipradilol, a beta-blocker having both vasodilating and alpha(1)-blocking activities, can protect retinal cells from the injury induced by ischemia and reperfusion. Rats were anesthetized and, after an intravitreal injection of nipradilol, the intraocular pressure was raised for 45 min to induce retinal ischemia and reperfusion. Before, and 3 and 7 days after the ischemia, electroretinograms were recorded. After the ischemia, the mean amplitude of the b-waves in rats receiving 5 microl of 1.0 x 10(-6) M nipradilol was significantly larger than of controls (injected with phosphate-buffered saline). Histologically, the reduction in the number of retinal ganglion cells (1.0 x 10(-6) M), and the thickness of the inner and outer plexiform layers and the inner nuclear layer (1.0 x 10(-6), 10(-7) and 10(-8) M) was suppressed by nipradilol. These results indicate that nipradilol protected the retina against retinal ischemia and reperfusion and should be considered for therapeutic use in cases of transient retinal ischemia.

Animals↗