Journal article
Behavioural and molecular consequences of chronic cannabinoid treatment in Huntington's disease transgenic mice
MJ Dowie, ML Howard, LFB Nicholson, RLM Faull, AJ Hannan, M Glass
Neuroscience | Published : 2010
Abstract
Early loss of CB1 receptors is a hallmark of human Huntington's disease. Data from rodent studies suggest that preservation and activation of CB1 receptors may be protective against disease progression. R6/1 transgenic mice are considered to be a model of early pathogenic changes in Huntington's disease. We have shown previously that levels of CB1 in R6/1 mice prior to the onset of motor symptoms (12 weeks of age) remain high enough to justify commencement of cannabinoid drug treatment. Eight weeks of daily treatment with the cannabinoid agonists HU210 (0.01 mg/kg) and δ9-tetrahydrocannabinol (THC, 10.00 mg/kg), or the inhibitor of endocannabinoid metabolism URB597 (0.30 mg/kg), did not alte..
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Funding Acknowledgements
We thank Jocelyn Bullock for assistance with tissue processing, Pritika Narayan and Mike Dragunow for assistance with analysis of ubiquitin aggregate data and Norac Pharma for gifting the THC. This work was supported by grants from the Neurological Foundation of New Zealand (M. G. and R.L.M.F.), the Australian National Health and Medical Research Council (A.J.H.) and a University of Auckland Health Research Doctoral Scholarship (M.J.D.).