Feed

Peripheral diabetic neuropathy (PDN) is a complication of diabetes mellitus that affects nerves and has great epidemiological and clinical relevance. It affects more than 2/3 of diabetic patients, compromising their quality of life and life expectancy. This chapter reviews the main electrophysiological alterations in excitability and conductibility observed in sciatic (somatic) and vagus (autonomic) nerves in experimental models of PDN, with emphasis on nerve extracellular recording. Initially, the clinical and pathophysiological aspects of PDN are outlined, followed by a brief review of experimental models of diabetes, particularly those induced by streptozotocin. The electrophysiological basis of compound action potential (CAP) generation is described, and key CAP parameters are discussed as indicators of functional nerve integrity. Experimental evidence demonstrates that diabetes induces consistent alterations in the sciatic nerve, characterized by reduced CAP amplitude and conduction velocity, increased duration of CAP waves, reflecting increased temporal dispersion of CAP components, and decreased nerve excitability. These changes worsen with disease duration and higher glycemic levels and may be detected even in pre-diabetic conditions. In contrast, the vagus nerve exhibits a more selective pattern of dysfunction. Recent experimental studies reveal that diabetes mellitus, at least at initial stages of disease evolution, preferentially affects myelinated vagal fibers, leading to reduced conduction velocity, increased component duration, and excitability, while unmyelinated fibers remain relatively preserved. Overall, the findings summarized in this chapter support the use of CAP recordings as a robust experimental approach for investigating the progression and mechanisms of PDN and for evaluating potential therapeutic interventions.