Subscribe to RSS
DOI: 10.1055/s-0032-1304567
Critical Evaluation of Mouse Models Used to Study Pain and Loss of Pain Perception in Diabetic Neuropathy
Publication History
received 17 January 2012
first decision 17 January 2012
accepted 30 January 2012
Publication Date:
08 March 2012 (online)
![](https://www.thieme-connect.de/media/eced/201204/lookinside/thumbnails/10.1055-s-0032-1304567-1.jpg)
Abstract
A number of studies have addressed diabetic neuropathy (DN) in transgenic and knock out mouse models to unravel the molecular mechanisms underlying metabolic pain and loss of pain perception. However, it is difficult to compare these studies with each other or even with human DN due to experimental differences including the type of diabetes, the background strain of the respective mouse model, the methods of diabetes induction and the duration of diabetes, animal age and gender. To receive useful information for DN from genetically modified mice, it is therefore mandatory to first define the appropriate model and – if necessary – to backcross transgenic strains into the respective background to allow a reliable (and at least in part translatable to human DN) interpretation of the results.
-
References
- 1 Tesfaye S, Boulton AJ, Dyck PJ et al. Diabetic neuropathies: update on definitions, diagnostic criteria, estimation of severity, and treatments. Diabetes Care 2010; 33: 2285-2293
- 2 Obrosova IG. Diabetic painful and insensate neuropathy: pathogenesis and potential treatments. Neurotherapeutics 2009; 6: 638-647
- 3 Sullivan KA, Lentz SI, Roberts Jr JL et al. Criteria for creating and assessing mouse models of diabetic neuropathy. Curr Drug Targets 2008; 9: 3-13
- 4 Mogil JS, Davis KD, Derbyshire SW. The necessity of animal models in pain research. Pain 2010; 151: 12-17
- 5 Dolgin E. Animalgesic effects. NatMed 2010; 16: 1237-1240
- 6 Langford DJ, Crager SE, Shehzad Z et al. Social modulation of pain as evidence for empathy in mice. Science 2006; 312: 1967-1970
- 7 Langford DJ, Bailey AL, Chanda ML et al. Coding of facial expressions of pain in the laboratory mouse. Nat Methods 2010; 7: 447-449
- 8 Chesler EJ, Ritchie J, Kokayeff A et al. Genotype-dependence of gabapentin and pregabalin sensitivity: the pharmacogenetic mediation of analgesia is specific to the type of pain being inhibited. Pain 2003; 106: 325-335
- 9 Jack MM, Ryals JM, Wright DE. Characterisation of glyoxalase I in a streptozocin-induced mouse model of diabetes with painful and insensate neuropathy. Diabetologia 2011; 54: 2174-2182
- 10 Jack MM, Ryals JM, Wright DE. Protection from diabetes-induced peripheral sensory neuropathy – A role of elevated glyoxalase I? Exp. Neurol 2011; DOI: 10.1016/j.expneurol.2011.12.015.
- 11 Bierhaus A, Fleming Th, Stoyanov S et al. Methylglyoxal modification of Nav1.8 facilitates nociceptive neuron firing and causes hyperalgesia in diabetic neuropathy. In revision. 2012
- 12 Homs J, Ariza L, Pagès G et al. Comparative study of peripheral neuropathy and nerve regeneration in NOD and ICR diabetic mice. Diabetes. J Peripher Nerv Syst 2011; 16: 213-227
- 13 Ii M, Nishimura H, Kusano KF et al. Neuronal nitric oxide synthase mediates statin-induced restoration of vasa nervorum and reversal of diabetic neuropathy. Circulation 2005; 112: 93-102
- 14 Sullivan KA, Hayes JM, Wiggin TD et al. Mouse models of diabetic neuropathy. Neurobiol Dis 2007; 28: 276-285