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Diabetic neuropathy is characterized by alterations in axonal excitability which can lead to either ‘positive’ or ‘negative’ symptoms (paraesthesiae and dysaesthesiae as compared to hypaesthesia and anaesthesia). At present, little is known about the mechanisms underlying such pathological changes in nerve function. Modification of axonal membrane conductances might be one factor involved. Hyperglycaemia and hypoxia are regarded as most important for the development of diabetic neuropathy (Low, 1987). This chapter reviews a series of studies in which the combined effects of hyperglycaemia and hypoxia have been tested on isolated peripheral myelinated axons. As compared with in vivo experiments using diabetic animals, such an in vitro model of diabetic neuropathy has enabled us to explore directly the effects of factors possibly involved in the pathogenesis of this disease on electro-physiological axonal parameters.
The in vitro nerve preparation
The effects of hyperglycaemic hypoxia were investigated using electro-physiological recordings from isolated rat dorsal and ventral roots. After isolation (Schneider et al., 1992), the spinal roots were incubated at room temperature for 30 minutes to about 8 hours in solutions with different concentrations of D-glucose or other hexoses. Afterwards these nerves were transferred to the experimental organ bath used to record compound action potentials, extracellular direct current (DC) potentials, and electrotonus (Marsh et al., 1987; Schneider et al., 1992, 1993b). It consisted of a three-chambered Plexiglas bath, into which the spinal root was sealed with silicone grease.