Peripheral Nerve Segmental Demyelination Induced by Intraneural Diphtheria Toxin Injection

Abstract

The compartmental equilibration of sodium Na 24 and carbon 14-labeled inulin was determined in hydrocortisone-treated (24 hours) and untreated rats in which segmental demyelination had been produced in one sciatic nerve by intraneural injection of diphtheria toxin. Diphtheria toxin caused increase in nerve water and sodium content, breakdown of the physiologic blood-nerve extracellular space (ECS) barrier to²⁴Na and inulin-¹⁴C, slowing of ECS-intracellular space (ICS) exchange of isotopic sodium, enlargement of the nerve ECS, and intracellular swelling. Hydrocortisone was found to restore the blood-nerve ECS barrier to isotopic sodium, reduce the water content of ECS and ICS, and slow blood-ECS exchange of inulin-¹⁴C (although it eventually distributed in nerve ECS at a level equal to that of untreated diphtheria toxin-injected nerve).