Neuropathy-functional abnormalities in the BB rat.
The spontaneously diabetic rat gets a decreased motor-nerve conduction velocity after the onset of diabetes as compared with age- and weight-matched controls. This finding has indicated that these rats develop a neuropathy; but morphological investigations have failed to show structural abnormalities that could explain the decrease in conduction velocity. Measurements of the nervous function revealed a decreased excitability of isolated fibers from sciatic nerves of rats with diabetes duration ranging from 18 days to 6 months. Voltage-clamp analysis of the membrane of the node of Ranvier showed (1) decreased Na-equilibrium potential, reflecting an axoplasmic Na accumulation; (2) decreased specific Na permeability, related both to an increased inactivation of the permeability of the resting node and also a decreased permeability when inactivation had been removed by hyperpolarization of the membrane; and (3) in some nodes a marked increase in the delayed K permeability, which is an early sign of paranodal demyelination. The decrease in Na permeability was the most important factor for the decreased nodal excitability and the decreased conduction velocity. This mechanism may also be involved in the reversible dysfunction found in human diabetic neuropathy.
D000200:Action Potentials; D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000503:physiopathology*; D003922:Diabetes Mellitus, Type 1 / Q000150:complications*; D003929:Diabetic Neuropathies / Q000503:physiopathology*; D005260:Female; D008297:Male; D008564:Membrane Potentials; D009413:Nerve Fibers, Myelinated / Q000378:metabolism / Q000502:physiology; D010539:Permeability; D011188:Potassium / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D012584:Sciatic Nerve / Q000503:physiopathology; D012964:Sodium / Q000378:metabolism
D012964:Sodium; D011188:Potassium