Population response of [Ca2+]i in cultured cortical astrocytes to excitatory amino acids was measured at room temperature using the calcium-sensitive dye fura-2. Quisqualic acid (QA), glutamate (Glu), and kainic acid (KA) caused a peak increase in [Ca2+]i in the order QA greater than Glu greater than KA. No response to N-methyl-D-aspartic acid (NMDA) was observed whether or not Mg2+ was present externally. Both QA and Glu (100 microM) frequently elicited a decaying oscillatory [Ca2+]i response during sustained agonist application; the period of oscillations initially was 23.5 sec and increased as the response was damped. Comparatively, the [Ca2+]i response to KA was nonoscillatory. Both responses to Glu and KA were reduced slightly by antagonist gamma- D-glutamylaminomethyl-sulfonic acid (1 mM), but virtually were abolished by kynurenic acid (3 mM). Replacement of external Na+ by choline had no significant effect on the Glu response. Removal of external Ca2+ reduced the peak response to QA, Glu, and KA to 40, 34, and 18%, respectively; and markedly reduced the degree of QA- and Glu- induced [Ca2+]i oscillations. Pretreatment with phorbol esters, a potent activator of protein kinase C, blocked the [Ca2+]i response to Glu but not KA. It is concluded that cortical astrocytes express Glu receptors of the non-NMDA type in culture and that receptor activation leads to Ca2+ influx and release of internal Ca2+. Mobilization of Ca2+ apparently occurs via the known Glu-mediated hydrolysis of inositol lipids, which may come under negative-feed-back control by protein kinase C activation. Oscillatory [Ca2+]i signaling offers the possibility of a dynamic population response in an electrically coupled glial network.
We have identified the glutamate receptor genes expressed by developing and adult rat optic nerve. Results from PCR suggested that of the ionotropic glutamate receptor (GluR) gene family, only GluR1 and GluR3 subunits are expressed by optic nerve. However, Northern blot analysis demonstrated that only the GluR1 subtype is expressed at appreciable levels. In situ hybridization histochemistry of GluR1 was performed and a diffuse pattern of expression was observed in both postnatal day 15 and adult optic nerve. Restriction mapping of the GluR1 PCR product indicated the expression of the flip alternative splice version in optic nerve. The detected GluR1 message was not due to axons because no loss of expression was observed after the degeneration of axons. PCR analysis also revealed the presence of a metabotropic glutamate receptor in optic nerve.
In a randomized design we examined whether endoscopists are biased by knowledge of the radiologic diagnosis of duodenal ulcer and deformity of the duodenal bulb when recording the corresponding endoscopic diagnoses. A total of 156 patients had a barium meal and were subsequently randomized into 2 groups. In 74 of the cases the 2 endoscopists knew the result of the X-ray examination when doing the endoscopy; in 82 of the cases they did not. One endoscopist was significantly biased by his knowledge of the radiologic diagnosis of deformity of the duodenal bulb. Neither of the endoscopists was biased by his knowledge of the radiologic diagnosis of duodenal ulcer. In addition, the interobserver variation between the two endoscopists with regard to the endoscopic diagnoses of duodenal ulcer, deformity of the duodenal bulb, and duodenitis was examined. The interobserver variation was expressed by the overall agreement and by the kappa statistics, which adjusts the overall agreement for expected chance agreement. For duodenal ulcer, deformity of the duodenal bulb, and duodenitis, the overall agreements and kappa values were 0.91, 0.78, and 0.75, and 0.54, 0.42, and 0.33, respectively.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.