In vitro and in vivo traumatic brain injury (TBI) alter the function and expression of glutamate receptors, yet the combined effect of these alterations on cortical excitatory synaptic transmission is unclear. We examined the effect of in vitro mechanical injury on excitatory synaptic function in cultured cortical neurons by assaying synaptically driven intracellular free calcium ([Ca(2+)](i)) oscillations in small neuronal networks as well as spontaneous and miniature excitatory postsynaptic currents (mEPSCs). We show that injury decreased the incidence and frequency of spontaneous neuronal [Ca(2+)](i) oscillations for at least 2 days post-injury. The amplitude of the oscillations was reduced immediately and 2 days post-injury, although a transient rebound at 4 h post-injury was observed due to increased activity of N-methyl-d-aspartate (NMDARs) and calcium-permeable α-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate receptors (CP-AMPARs). Increased CP-AMPAR function was abolished by the inhibition of protein synthesis. In parallel, mEPSC amplitude decreased immediately, 4 h, and 2 days post-injury, with a transient increase in the contribution of synaptic CP-AMPARs observed at 4 h post-injury. Decreased mEPSC amplitude was evident after injury, even if NMDARs and CP-AMPARs were blocked pharmacologically, suggesting the decrease reflected alterations in synaptic Glur2-containing, calcium-impermeable AMPARs. Despite the transient increase in CP-AMPAR activity that we observed, the overriding effect of mechanical injury was long-term depression of excitatory neurotransmission that would be expected to contribute to the cognitive deficits of TBI.

mechanism for spheroplast formation in Bacillus cereus and Escherichia coli. J. Bacteriol. 90:1355-1364. 1965.-Spheroplasts of Bacillus cereus strain T and Escherichia coli B were prepared by incubating early log-phase cells in appropriate buffers and stabilizers for 3 hr at 30 and 37 C, respectively. Upon incubation in 0.05 M tris(hydroxymethyl)aminomethane buffer osmotically stabilized with 16% polyethylene glycol at pH 7.5, 99% of the B. cereus cells formed spheroplasts; 90% of the E. coli cells were converted to spheroplasts in 0.4 M sodium acetate buffer osmotically stabilized with 1.6 M sucrose at pH 6.0. The extent of spheroplast formation was determined by phase-contrast microscopic examination, by measuring the rate of fall of optical density in the reaction mixture when subjected to osmotic shock, and by viable intact cell counts. The effect of a selected group of metabolic inhibitors on the autolytic system of B. cereus and E. coli has been examined. B. cereus and E. coli wall components comprising 26% of the dry weight of the original cellular material were recovered from dialyzed fractions by precipitation in 70% ethyl alcohol. Chemical and chromatographic analysis of cell-wall hydrolysates from B. cereus and E. coli indicated the presence of glucosamine, alanine, lysine, glycine, aspartic acid, diaminopimelic acid, glutamic acid, and muramic acid.

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PROTEIN COMPONENT OF ENDOTOXINblood glucose must be maintained for a certain period before its reduction to stimulate HGH secretion.Oufr observation is difficult to interpret, but raises some questions on the regulatory manner of HGH secretion mlediated by glucose metabolism. If the stimulation of HGH secretion CUTS by intracellular glucose deprivation( 1-3) in the hypothalamus( 2,7) as proposed, glucose infused for a short period in most cases is unable to induce enough metabolic shift in the hypothalamic cells to stimulate HGH secretion, in spite of other definite responses such as plasna NEFA change. An alternative explanation may be that the direct stimulant of HGH secretion is not the extracellular or intracellular glucose itself, but the metabolites or other substances related to glucose metabolism, which are different quanrtitatively or qualitatively in the conditions of Short and long continuous glucose infusion. Since plasma NEFA change was similar in all cases, it is apparent that there is no conrelation between the rise of plasma HGH and the value of plasma NEFA. In these respects, our results may support the observation of Quabbe et aZ (8), who showed the absence of correlation between plasma HGH rise and blood glucose or plasma NEFA level during a 24-hour fast in normal subjects.Summary. Serial plasma HGH concentrations were measured, in 18 normal subjects, following continuous intravenous glucose in-fusion performed for periods of 3, 10, 20 and 30 minutes. In 5 of 8 cases infused for 3 minutes, no rise of plasma HGH was olbserved in spite of the rapid fall of blood glucose with (4 cases) or without (1 case) its reduction below the fasting level. The 3 other cases infused for 3 minutes and all 10 cases of 10, 20 and 30 minutes' infusion showed definite rise of plasma HGH at 90-180 minutes following the infusion. From the results obtained, it appears that the falling blood glucose per se is not a direct stimulus, and the reduction of blood glucose !below the fasting level is not necessarily a stimulus to HGH secretion.

A Boivin preparation of Brucella abortus, unlike common enterobacterial endotoxins, failed to depress water intake or increase numbers of hemolysin-producing spleen cells in mice, or to cause delayed inflammatory reactions in rabbit skin. Reactivity to the B. abortus endotoxin was found only in animals which were previously given the endotoxin with, but not necessarily in, complete Freund's adjuvant. Previous treatment with the endotoxin in saline or with only the adjuvant was ineffective. Sensitization appeared within 10 days and waned after 5 weeks. Passive sensitization was obtained with sensitized donor spleen cells but not with serum. Serum antibody titers did not correlate with the appearance and disappearance of sensitization.