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The effects of temporal inactivation of the CA3-region was examined in a non-associative task, the spatial open-field, designed to estimate the ability of mice to react to spatial changes, and in the object recognition task, designed to estimate the ability of mice to identify a familiar object.
Left untreated, the latency of Fabry-Rag mice to react to the hot-plate essentially doubled over the eight months of the experiment.
We next tested the capability of Kb+/+Db+/+ (wild-type B6) mice to react to the decreased expression levels of MHC class I on target cells from Kb+/−Db+/− mice.
We tested the reactivity of peripheral blood lymphocytes (PBLs) from unprimed lupus mice to react with RNP1-containing peptides from several spliceosomal proteins.
The ability of anti-STn sera raised in MUC1 TG mice to react with various STn-positive proteins was analysed by western blotting.
To exclude that the observed differences were due to an altered ability of NCR1gfp/gfp mice to react to an unspecific irritation, the ears of mice were treated with the irritant benzalkonium chloride.
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Potential therapeutics can be evaluated in this model for their effects on a nociceptive response to a heat stimulus by measuring the time taken by the mouse to react (latency) after being placed on a 55°C hot-plate.
We chose this dose since it did not blunt heart rate reactivity during air-jet stress, allowing the mouse to react normally to a stressful situation.
In this case, the mice failed to react with raised levels of AMPK, showing that the stimulation of the enzyme by the drug depends on the stimulation of the H1 histamine receptor, the researchers report online this week in the Proceedings of the National Academy of Sciences.
This effect is probably due to the inability of mouse cytokines to react with human receptors, leading to survival signal and trophic factor deprivation in transplanted human cells.
In general, rats and mice are believed to react in rather similar manners to brain ischemia.
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