Effects of Methylprednisolone on Axonal Depression Induced by Hypoxia, ??-Aminobutyric Acid, and (??)-8-Hydroxy-Dipropylaminotetralin Hydrobromide

Abstract

OBJECTIVE We sought to confirm the effects of methylprednisolone (MP) on axonal depression induced by hypoxia, γ-aminobutyric acid (GABA), and (±)-8-hydroxy-dipropylaminotetralin hydrobromide (8-OH-DPAT). METHODS Compound action potentials were recorded to assess the effects of MP in neonatal rat spinal cord axons. Longitudinally hemisected spinal cords were superfused for 120 minutes in Ringer’s solution saturated with 95% N2 and 5% CO2. The effect of MP on GABA- and 8-OH-DPAT-induced axonal depression was analyzed with oxygenated isolated dorsal columns. RESULTS Hypoxia (120 min) significantly reduced the response amplitudes in hemicord preparations. MP (30 μmol/L) prevented hypoxia-induced depression of action potential amplitudes. In oxygenated dorsal column preparations, GABA (50 μmol/L) significantly reduced action potential amplitudes. At 10, 30, and 100 μmol/L, MP had no effect on axonal excitability and GABA-induced axonal depression. 8-OH-DPAT (100 μmol/L) significantly reduced the action potential amplitude. MP (10, 30, 50, and 100 μmol/L) reduced 8-OH-DPAT-induced amplitude depression in a dose-dependent manner. CONCLUSION At the higher concentrations, MP protected spinal cord axons against hypoxia-induced excitability loss. It had an effect on serotonin 1A-induced axonal depression but not on GABA-induced depression.