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Nigranoic acid, a new seco-triterpenoid, was isolated from Shizandra nigra and proved to be 3,4-seco-9,19-cyclo-9β-lanosta-4(28),24-dien-3,26-dioic acid (I).

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ABSTRACT. i -Gliitamate, a putative photoreceptor cell neurotransmitter, causes thinning of the inner layers of the retina and has been used for preparing biologically fractionated photoreceptor cells. However, it is possible that absence of the inner retinal layers may affect the remaining retina, and/or glutamate may directly affect photoreceptor cells. Weevaluated quantitatively the effects of i -glutamate on the developing photoreceptor cells by measuring the rod photoreceptor cell-specific protein, opsin. Wepurified rat rhodopsin and used it as the standard for measuring opsin content of rat retinas with competitive enzyme-linked immunosorbentassay. Various concentrations of glutamate were injected into 7-day-old rats, and the effects of the amino acid concentration on opsin expression were determined on postnatal day 14. Inner layers of the retina degenerated when10 ju\ or 15 ju\ of 2.4 M glutamate/gram body weight was administered subcutaneously. Opsin content of these glutamate-treated retinas decreased significantly compared with control retinas. Weadministered glutamate to rats at various stages of development and determined the effects by light microscopy on postnatal day 14. The administration of glutamate resulted in no degeneration of the inner retina if injected on postnatal day 1 or 2, degeneration of the inner retina between day 3 to 7, and again, no degeneration after postnatal day 13. Opsin content decreased significantly when glutamate was administered between postnatal day 1 to 7, but not after day 13, the day the blood-retinal barrier seems to reach maturity. Our findings indicate that systemic administration of L-glutamate affects the expression of opsin in the developing rod photoreceptor cells.Glutamate is a leading candidate for the excitatory neurotransmitter of the vertebrate retinal photoreceptors (2, 4, 10) and bipolar cells (8,15,26). Neurotoxicity by endogenous excitatory amino acids such as glutamate has been implicated as a mechanism for central (24) and retinal neuronal cell loss (29) after ischemia.Moreover, it is shown that an abnormality in the glutamate metabolism may cause a retinal dysfunction (1).Since Lucas and Newhouse(13) reported the toxic effects of glutamate on the inner retina, the amino acid has been used to prepare biologically fractionated photoreceptors since the photoreceptors appeared normal in form and concentration. The results using the fractionated photoreceptors provided important clues to amino acid levels (6), electroretinograms (21), and distribution of the enzymes (22) In the present study, to evaluate the effects of neurotoxic glutamate on the developing rat photoreceptor cells quantitatively, an assay of the rod photoreceptorspecific protein, opsin, in glutamate-administered rat retinas was carried out.

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