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Electronic control devices (ECDs) may eventually be deployed by the military in a manner resulting in longer exposures than those encountered during law-enforcement operations. In a previous study, 18 repeated cycling (5-second on/5-second off) exposures (within a 3-minute period) of anesthetized swine to an ECD (TASER International's Advanced TASER X26 device) resulted in leg muscle contraction, acidosis, and increases in blood electrolytes. In the current study, experiments were performed to examine effects of exposures to a different cycling rate (7-second on/3-second off), from a modified X26 ECD, on 10 swine (Sus scrofa), maintained on propofol anesthesia. In contrast with the previous study, a large number of animals (6/10) died immediately after the exposures. There were no major differences in pre-exposure blood factors from survivors versus nonsurvivors, with the exception of hematocrit and 2 isoenzymes of lactate dehydrogenase. It is doubtful that these factors would be useful in predicting survival after ECD exposure. Blood pH was significantly decreased after exposure, but (in animals that survived) subsequently returned to baseline levels. On the basis of the overall survival rate, further development of useful ECDs (for long-term incapacitation during military operations) may require consideration of longer pauses between repeated exposures over a 3-minute period.

When infused in rats, rotenone, a mitochondrial complex I inhibitor, induces alterations that resemble the histological changes of Parkinson's disease, particularly degeneration of the nigrostriatal dopaminergic system. However, the specificity of rotenone effects has been challenged recently. We have re-examined the alterations caused by rotenone in the substantia nigra and the striatum of rats after infusion of rotenone (2 mg/kg per day s.c.) for 21 days. Three patterns of striatal tyrosine-hydroxylase immunoreactivity (TH-IR) were observed: 46% of animals showed no reduction, and 46% of animals showed diffuse reduction in TH-IR, whereas one animal presented a focal loss of TH-IR in the striatum. Confocal microscopy analysis showed that the vesicular monoamine transporter (VMAT2) was decreased in parallel with TH-IR, strongly suggesting a loss of striatal DA nerve terminals in animals with diffuse or central TH-IR loss. However, no significant loss of TH-IR neurons was observed in the substantia nigra. Analysis of NeuN and DARPP-32 immunoreactivity, and Nissl staining, in the striatum showed no striatal neuronal loss in animals with either preserved TH-IR or diffuse TH-IR reduction. However, in the animal with focal TH-IR loss, severe neuronal loss was evident in the center and the periphery of the striatum, together with microglial activation detected by OX-6 and OX-42 staining. Thus, in most cases, chronic subcutaneous infusion of low doses of rotenone does not induce significant striatal neuronal loss, despite TH-IR and VMAT-IR reduction in a subset of animals, supporting the use of rotenone as a model of Parkinson's disease under carefully controlled experimental conditions.

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