Genetic studies have implicated the evolutionary novel, anthropoid primate-specific gene locus G72/G30 in psychiatric diseases. This gene encodes the protein LG72 that has been discussed to function as a putative activator of the peroxisomal enzyme D-aminoacid-oxidase (DAO) and as a mitochondrial protein. We recently generated 'humanized' bacterial artificial chromosome transgenic mice (G72Tg) expressing G72 transcripts in cells throughout the brain. These mice exhibit several behavioral phenotypes related to psychiatric diseases. Here we show that G72Tg mice have a reduced activity of mitochondrial complex I, with a concomitantly increased production of reactive oxygen species. Affected neurons display deficits in short-term plasticity and an impaired capability to sustain synaptic activity. These deficits lead to an impairment in spatial memory, which can be rescued by pharmacological treatment with the glutathione precursor N-acetyl cysteine. Our results implicate LG72-induced mitochondrial and synaptic defects as a possible pathomechanism of psychiatric disorders.

Plasma levels of local anaesthetics following their injection are affected by many factors. Serial plasma levels following injection of lignocaine and prilocaine at various rates in over 500 patients have been measured and this has allowed some of these factors to be assessed and quantified. The vascularity of the site of injection causes major differences in the maximum plasma level. Prilocaine consistently gives lower levels than lignocaine. Adrenaline causes a reduction in the plasma levels of both drugs and the optimal concentration is 1:200,000. Speed of injection is important when giving the drugs intravenously but not epidurally. The concentration of the injected solution does not affect the plasma levels. The weight and age of the patients (all adult females) were unrelated to the mayi'mnm plasma levels.

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