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I think the work on the schizophrenic mouse model is interesting. It is impressive that the researchers have developed a model where a relevant gene, the dopamine receptor is expressed in the relevant part of the brain, the striatum and that the gene can be swithced off with an antibiotic switch. I would like to know more about how they did this, is the gene on a plasmid or integrated into the mouse chromosomes? It was particularly interesting that having generated the symptoms of deficits in working memory by expressing the gene, no benefit was observed in the mice when the gene was switched off. This raises practical and ethical issues about early testing for people with a family history of schizophrenia. It is of course salient that the neurophysiology of mice and men differ significantly and that many key symptoms of schizophrenia such as hallucinations and delusions are impossible to measure in mice.