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Two types of mammalian direction-selective ganglion cells (DSGCs), ON and ONOFF, operate over different speed ranges. The directional axes of the ON-DSGCs are thought to align with the axes of the vestibular system and provide sensitivity at rotational velocities that are too slow to activate the semicircular canals. ONOFF-DSGCs respond to faster image velocities. Using natural images that simulate the natural visual inputs to freely moving animals, we show that simulated visual saccades suppress responses in ON-DSGCs but not ONOFF-DSGCs recorded in retinas of domestic rabbits of either gender. Analysis of the synaptic inputs shows that this saccadic suppression results from glycinergic inputs that are specific to ON-DSGCs and are absent in ONOFF-DSGCs. When this glycinergic input is blocked, both cell types respond similarly to visual saccades and display essentially identical speed tuning. The results demonstrate that glycinergic circuits within the retina can produce saccadic suppression of retinal ganglion cell activity. The cell-type-specific targeting of the glycinergic circuits further supports the proposed physiological roles of ON-DSGCs in retinal-image stabilization and of ONOFF-DSGCs in detecting local object motion and signaling optical flow. In the mammalian retina, ON direction-selective ganglion cells (DSGCs) respond preferentially to slow image motion, whereasONOFF-DSGCs respond better to rapid motion. The mechanisms producing this different speed tuning remain unclear. Here we show that simulated visual saccades suppress ON-DSGCs, but not ONOFF-DSGCs. This selective saccadic suppression is because of the selective targeting of glycinergic inhibitory synaptic inputs to ON-DSGCs. The different saccadic suppression in the two cell types points to different physiological roles, consistent with their projections to distinct areas within the brain. ON-DSGCs may be critical for providing the visual feedback signals that contribute to stabilizing the image on the retina, whereas ONOFF-DSGCs may be important for detecting the onset of saccades or for signaling optical flow.

Background-A previous study showed that the glucocorticoid dexamethasone, at doses of 100 µg/kg and above, inhibited leucocyte adhesion to rat mesenteric postcapillary venules activated with interleukin 1 (IL-1 ), as assessed by videomicroscopy. Aims-To identify whether the adhesion molecule, intercellular adhesion molecule 1 (ICAM-1), or the chemokine KC could be targeted by the steroid to mediate its antiadhesive eVect. Methods-Rat mesenteries were treated with IL-1 (20 ng intraperitoneally) and the extent of leucocyte adhesion measured at two and four hours using intravital microscopy. Rats were treated with dexamethasone, and passively immunised against ICAM-1 or KC. Endogenous expression of these two mediators was validated by immunohistochemistry, ELISA, and the injection of specific radiolabelled antibodies. Results-Dexamethasone greatly reduced IL-1 induced leucocyte adhesion, endothelial expression of ICAM-1 in the postcapillary venule, and release of the mast cell derived chemokine KC. Injection of specific antibodies to the latter mediators was also extremely eVective in downregulating (>80%) IL-1 induced leucocyte adhesion. Conclusions-Induction by IL-1 of endogenous ICAM-1 and KC contributes to leucocyte adhesion to inflamed mesenteric vessels. Without excluding other possible mediators, these data clearly show that dexamethasone interferes with ICAM-1 expression and KC release from mast cells, resulting in suppression of leucocyte accumulation in the bowel wall, which is a prominent feature of several gastrointestinal pathologies. (Gut 1999;45:705-712)

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SUMMARY : Washed suspensions of a laboratory strain of Haernophilus pertussis did not take up oxygen with, or ferment, five carbohydrates, nor did the same strain produce detectable acid from fourteen carbohydrates during growth. Of twenty-one amino-acids tested only proline, serine, alanine, aspartic and glutamic acids were oxidized by washed suspensions a t an appreciable rate. The first four of these were oxidized to completion but with glutamic acid only 80 yo of the theoretical uptake of oxygen occurred ; however, in the presence of dinitrophenol it, too, was oxidized to completion. Cells oxidizing glutamic acid in the presence of arsenite produced a-ketoglutaric acid.During the logarithmic growth of H . pertussis glutamic acid disappeared from Cohen & Wheeler's medium. The organism grew in a Cohen & Wheeler's medium in which the Casamino acids had been replaced by glutamic acid. These results suggest that glutamic acid can serve as energy, carbon and nitrogen source for H . pertussis.