engleski

ALTERED INWARD RECTIFICATION IN MYELINATED SENSORY AXONS OF STREPTOZOTOCIN (STZ)-DIABETIC RATS

Diabetic neuropathy is one of he most common complication of long term diabetes. At the present, little is knowm about the possible mechanisms involved in the pathological changes in nerve function, however modification of axonal membrane conductances might be one of the factors involved. The aim of our study was to examine rectifying and steady state properties of large myelinated axons from isolated sural nerves in control and diabetic rats. Experiments were performed on STZ-treated ( 45 mg/kg i.p. 3 days in the row ) Sprague Dawley male rats ( 3 months after STZ treatment ) and age matched controls. Intracellular recordings were obtained using standard current-clamp technique. Potassium channel blockers were applied by diffusion from 3M KCI recording microelectrode containing 50mM 1-AP and 20 mM TEA ( D.C. resistance > 80 Mohm), and CsCl (3 mM) was added into a perfusing Ringer. Sensory axons of diabetic rats revealed decrease in conduction velociy (17.86 ą 3.81 m/s vs. 28.92 ą 1.55 m/s, mean ą SE for control). Quantitative analysis of input resistance in response to hyperpolarization revealed significant decrease in steady state resistance (hRss) values ( 35.29 ą 2.63Mohm, for control. vs. 45.05 ą 5.01 Mohm mean ą SE, control n=17, STZ n=2 ), suggesting for significant inerease in inward rectification (IR). Similar hRss values were obtained in control axons after application of 3mM CsCl. Our study demonstrates that one of the early signs of diabetic neuropathy is selective defect of' IR in large myelinated sensory axons suggesting that pharmacological modulation of that internodal ionic conductance possible may have some clinical relevance.

diabetic neuropathy; streptozotocin; rats

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