Chemical synapses equipped with ribbons are tonically active, high-output synapses. The ribbons may play a role in the trafficking of synaptic vesicles. Recent findings in retinal rod cells of BALB/c mice indicate that ribbons are large and smooth in the dark phase, and, due to the formation and release of protrusions, small during the light phase. As a consequence of these changes, ribbons may traffick fewer vesicles in the light than in the dark phases. The aim of the present study was to find out whether the above ribbon changes in this mouse strain are strictly illumination-dependent and which signalling processes may be involved. Here, we show that ribbons form protrusions and release them into the cytoplasm within 30-60 min after lights on, the reverse occurring within 30 min after lights off. Under constant light or constant dark, no circadian rhythm of synaptic ribbon changes is observed. The illumination-dependence of ribbon structure is supported by in vitro experiments showing that in dark-adapted retinas, light induces the same morphological changes as in vivo. In vitro, the effect of light on the ribbons can be counteracted by cyclic guanosine monophosphate and melatonin. In dark-adapted retinas, light effects can be produced by decreasing the calcium ion concentrations in the incubation media. These results suggest that in retinal rod cells, the well known phototransduction signalling mechanisms may be responsible for the ribbon changes presently and previously reported.

In experimental designs of animal models, memory is often assessed by the time for a performance measure to occur (latency). Depending on the cognitive test, this may be the time it takes an animal to escape to a hidden platform (water maze), an escape tunnel (Barnes maze) or to enter a dark component (passive avoidance test). Latency outcomes are usually statistically analyzed using ANOVAs. Besides strong distributional assumptions, ANOVA cannot properly deal with animals not showing the performance measure within the trial time, potentially causing biased and misleading results. We propose an alternative approach for statistical analyses of latency outcomes. These analyses have less distributional assumptions and adequately handle results of trials in which the performance measure did not occur within the trial time. The proposed method is well known from survival analyses, provides comprehensible statistical results and allows the generation of meaningful graphs. Experiments of behavioral neuroscience and anesthesiology are used to illustrate this method.

No abstract

While low concentrations of S(+) ketamine allow an ischemia-induced increase in the number of new neurons, high S(+) ketamine concentrations block the post-ischemic increase in newly generated neurons. This effect is irrespective of the extent of other histopathological damage and in line with studies showing that NMDA receptor antagonists like MK-801 inhibit neurogenesis after cerebral ischemia.

Background: Postischemic endogenous neurogenesis can be dose-dependently modulated by volatile anesthetics. The intravenous anesthetic propofol is used during operations with a risk of cerebral ischemia, such as neurosurgery, cardiac surgery, and vascular surgery. The effects of propofol on neurogenesis are unknown and, therefore, the object of this study.Methods: Eighty male Sprague-Dawley rats were randomly assigned to treatment groups with propofol administration for 3 h: 36 mg · kg ؊1 · h ؊1 propofol with or without cerebral