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The reactivity of rare-earth sesquioxides, mainly neodymium oxide, in water vapor and their hydration process have been investigated by measuring the adsorbed amounts, infrared spectra, and water contents. The adsorption of water vapor on neodymium oxides, A-type and C-type Nd2O3, led to the formation of a neodymium hydroxide, Nd(OH)3. The variation of adsorbed amounts (in weight) with exposure time to water vapor suggested that the hydration process is different depending upon the crystal structure of neodymium sesquioxides. Combining with the data of IR spectra and water contents, it has been revealed that the hydration of A-type Nd2O3 takes place in one step [into Nd(OH)3] after an induction period of about 30 min, while that of C-type Nd2O3 proceeds in two steps [into Nd(OH)3 via NdOOH]. The adsorption of water vapor on other rare-earth sesquioxides was also examined; the hydration process of A-type lanthanum oxide (La2O3) was similar to that of A-type Nd2O3, while those of C-type sesquioxides, Nd2O3, samarium oxide (Sm2O3), and yttrium oxide (Y2O3), were different from each other. The difference in the rates of hydration for these oxides can be correlated with a basic nature of oxide. Therefore, the rate of hydration is eventually governed by the ionic radius of rare-earth metal ion because the basicity of oxide depends on the ionic radius of metal ion. To make the Nd2O3 surface resistant to water, the surface modification or coating was also tried by adsorbing a metal-alkoxide vapor. As a result, it was revealed that the surface-coated neodymium oxide (i.e., titania-coated Nd2O3) has a water-resistant property.

It had been thought that quantal size in synaptic transmission is invariable. Evidence has been emerging, however, that quantal size can be varied under certain conditions. We present evidence that alteration in vesicular [(3)H]L-glutamate (Glu) content within the synaptosome (a pinched-off nerve ending preparation) leads to a change in the amount of exocytotically released [(3)H]Glu. We found that Rose Bengal, a polyhalogenated fluorescein derivative, is a quite potent membrane-permeant inhibitor (K(i) = 19 nM) of glutamate uptake into isolated synaptic vesicles. This vesicular Glu uptake inhibition was achieved largely without affecting H(+)-pump ATPase. We show that various degrees of reduction elicited by Rose Bengal in [(3)H]Glu in synaptic vesicles inside the synaptosome result in a corresponding decrease in the amount of [(3)H]Glu released in a depolarization- (induced by 4-aminopyridine) and Ca(2+)-dependent manner. In contrast, fluorescein, the halogen-free analog of Rose Bengal, which is devoid of inhibitory activity on vesicular [(3)H]Glu uptake, failed to change the amount of exocytotically released [(3)H]Glu. These observations suggest that glutamate synaptic transmission could be altered by pharmacological intervention of glutamate uptake into synaptic vesicles in the nerve terminal, a new mode of synaptic manipulation for glutamate transmission.