We have been studying the role of the brainstem Pedunculopontine nuclei (PPN) in the control of locomotion and posture. Our results show that in the intact normal monkey low frequency (10 Hz) stimulation of the PPN increases motor activity significantly, whereas high frequency stimulation reduces it. Giving the monkey MPTP produces Parkinsonian akinesia, but we have shown that this can be alleviated by injecting bicuculline or by unilateral low frequency electrical stimulation in the PPN. These results imply that Parkinsonian akinesia is at least partly the result of excessive inhibition of the PPN by descending GABAergic projections from the basal ganglia that can be by-passed by stimulating the PPN directly. The increase in movements probably occurs both by stimulating the PPNs ascending projections to engage surviving dopaminergic mechanisms in the basal ganglia, but also by stimulating PPN projections descending to brainstem locomotor and postural centres, downstream from the dopaminergic systems (Nandi et al. 2002a,b; Jenkinson et al. 2004, 2005). What is really exciting is that these results suggested strongly that PPN stimulation might be clinically effective in treating akinesia in advanced Parkinsons disease and other akinetic disorders. Late in the disease many patients develop akinesia that is not alleviated by any current drug or deep brain stimulation treatment (Kleiner-Fisman et al. 2003), but our results suggested that PPN stimulation might change all this. This problem is so serious that, already on the basis of our monkey findings, two groups have implanted stimulating electrodes in the PPN in akinetic Parkinsonian patients (Mazzone et al. 2005; Plaha & Gill, 2005). Both studies show that low (10 Hz) frequency stimulation of the PPN, as predicted from our monkey experiments, greatly alleviates the gait freezing and postural instability of Parkinsonian patients that is both so highly disabling and resistant to conventional surgery. We have described the effects of PPN stimulation combined with L-Dopa therapy in the Parkinsonian monkey (Jenkinson et al. 2005). We confirm that driving the PPN at 10 Hz does alleviate akinesia at least partly via a non-dopaminergic pathway (Jenkinson et al. 2005). This rapid translation of monkey experiments in the laboratory to the alleviation of human suffering in the clinic confirms our belief in the enormous value of animal research to the human condition. It is particularly important to emphasise this at a time when animal experiments are so strongly under attack in the UK.