Nodal gap substance in diabetic nerve.
Anoxia and KC1 have been used to inactivate peripheral nerves by depolarization conduction block. Investigation of the inactivation patterns in isolated sciatic nerves of healthy and alloxan-diabetic rats suggests that the paranodal gap substance of healthy nerve behaves as an effective periaxonal diffusion barrier. In diabetic nerve the permeability of this barrier is significantly increased. A marked reduction in the K' binding capacity of the nodal gap substance has been demonstrated in myelinated nerves of human diabetics and alloxan diabetic rats.
D000818:Animals; D002463:Cell Membrane Permeability; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism / Q000503:physiopathology*; D003929:Diabetic Neuropathies / Q000378:metabolism / Q000503:physiopathology*; D004058:Diffusion; D004558:Electric Stimulation; D005071:Evoked Potentials; D006025:Glycosaminoglycans / Q000378:metabolism*; D006801:Humans; D000860:Hypoxia / Q000503:physiopathology; D008564:Membrane Potentials; D009186:Myelin Sheath / Q000378:metabolism / Q000502:physiology; D009431:Neural Conduction; D010525:Peripheral Nerves / Q000503:physiopathology*; D011188:Potassium / Q000378:metabolism; D011901:Ranvier's Nodes / Q000378:metabolism*; D051381:Rats; D012584:Sciatic Nerve / Q000378:metabolism / Q000503:physiopathology
D006025:Glycosaminoglycans; D011188:Potassium