title: Nodal gap substance in diabetic nerve.
abstract: 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.
mesh_terms: 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
chemical_list: D006025:Glycosaminoglycans; D011188:Potassium