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Since MEXX showed potent inhibition activity against ChE enzymes in the primary experiments with the IC50 value of 16.17 μg/mL, the in vivo effects of MEXX on scopolamine-induced memory deficit were investigated by using the Y-maze task.
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Among them the hippocampal dependent memory deficit is well known.
The composite score, termed "working memory deficit," is calculated by subtracting the average of the copying trials from the average of the delay trials.
The composite score, termed 'working memory deficit,' is calculated by subtracting the average of the copying trials from the average of the delay trials.
The memory deficit was confirmed by a probe test performed at the end of the learning sequence.
As suggested by the data in the two previous tests, the remote memory deficit was moderate but significant.
In schizophrenic subjects, working memory deficit is permanent and stable even when their clinical symptoms are largely in remission [10], [11].
While a recent study suggests that risperidone may worsen working memory in first episode patients, the same study also reported that the working memory deficit is already present before medication is administered [74].
For example, it remains unclear if the neural recruitment observed almost universally in cross-sectional "activation" studies of working memory deficit is due to formal brain reorganization or is indicative of neural inefficiency during periods of cognitive challenge [12], [13].
Comparisons with their wild type controls show that the remote memory deficit was again observed in the Itgβ2−/−, Soat1−/− and Syn2−/− mice (Figure 3b, c and d, respectively) and that they had normal STM.
However, the short-term memory deficit is not specific to spatial information in GluA1−/− mice [7,8].
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