Approximately 10% of total zinc in the brain exists in synaptic vesicles of glutamatergic neurons; however, the function of vesicular zinc is poorly understood. The presynaptic action of zinc against excitatory and inhibitory neurotransmission was studied in rat hippocampus using in vivo microdialysis. When the hippocampal CA3 region was perfused with 10-300 microM ZnCl(2), the level of glutamate in the perfusate was decreased, whereas the level of gamma-aminobutyric acid (GABA) was increased. Chelation of endogenous zinc with CaEDTA increased the glutamate level in the perfusate but decreased the GABA level, suggesting that zinc released into the synaptic cleft acts differentially on glutamatergic and GABAergic neurons in the CA3 region. The increase of GABA level by zinc was antagonized by 2,3-dioxo-6-nitro-1,2.3,4-tetrahydrobenzo(f)quinoxaline-7-sulphonamide (NBQX), an antagonist of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA)/kainate receptors, but not affected by MK801, an antagonist of N-methyl-D-aspartate (NMDA) receptors, and verapamil, a blocker of voltage-dependent calcium channels. The present study suggests that zinc enhances GABA release via potentiation of AMPA/kainate receptors in the CA3 region, followed by a decrease in presynaptic glutamate release in the same region. Zinc seems to be an inhibitory neuromodulator of glutamate release.
Chenopodium album has a non-photosynthetic chlorophyll protein known as the water-soluble chlorophyll (Chl)-binding protein (WSCP). The C. album WSCP (CaWSCP) is able to photoconvert the chlorin skeleton of Chl a into a bacteriochlorin-like skeleton. Reducing reagents such as β-mercaptoethanol or dithiothreitol inhibit photoconversion, indicating that S–S bridge(s) in CaWSCP are quite important for it. Recently, we found that the mature region of CaWSCP contains five cysteine residues; Cys2, Cys30, Cys48, Cys63, and Cys144. To identify which cysteine residues are involved in the photoconversion, we generated five mutants (C2S, C30S, C48S, C63S, and C144S) by site-directed mutagenesis. Interestingly, C48S, C63S, and C144S mutants showed the same Chl-binding activity and photoconvertibility as those of the recombinant wild-type CaWSCP-His, while the C2S and C30S mutants completely lost Chl-binding activity. Our findings indicated that the S–S bridge between Cys2 and Cys30 in each CaWSCP subunit is essential for Chl-binding activity.
Background Few studies have reported on the effects of the energy expenditure estimated from the frequency of exercise on bone mass, bone metabolic marker and bone related hormones in young females. The goal of this study is to examine the indices related to bone metabolism such as the bone metabolism markers and hormones and clarify their association with the bone mass through their relationship to exercises. Methods A total of 190 premenopausal Japanese females aged 20-49 years participated in this study. The calcaneus stiffness index (SI) was measured by ultrasound bone densitometry. The subjects' past and present exercise was measured using the self-administered questionnaire. Urinary deoxypyridinoline (DPD), 1,25-dihydroxyvitamin D3, intact parathyroid hormone (PTH), and bone specific alkaline phosphatase (BAP) were determined. Results DPD was shown to be a strong negative predictor of the SI (p<0.05). Energy expenditure by exercise only during senior high school in the exercise history was shown to be a positive predictor of the SI (p<0.05). Energy expenditure by exercise only during senior high school was shown to be a significant negative predictor of the DPD (p<0.05). Conclusion It has been revealed that the amount of energy expenditure from physical activity during the subject's high school years affects the levels of SI and DPD in adulthood.
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