Journal
ANESTHESIOLOGY
Volume 104, Issue 2, Pages 338-343Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/00000542-200602000-00020
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Background: Although intrathecal administration of midazolam, a water-soluble imidazobenzodiazepine derivative, has been found to produce analgesia, how it exerts this effect at the neuronal level in the spinal cord is not fully understood. Methods: The effects of midazolam on electrically evoked and spontaneous excitatory transmission were examined in lamina H neurons of adult rat spinal cord slices using the whole cell patch clamp technique. Results: Bath-applied midazolam (1 mu m) diminished A delta- and C-fiber evoked polysynaptic excitatory postsynaptic currents in both amplitude and integrated area. However, it affected neither A delta- and C-fiber evoked monosynaptic excitatory postsynaptic currents in amplitude nor miniature excitatory postsynaptic currents in amplitude, frequency, and decay time constant. In the presence of a benzodiazepine receptor antagonist, flumazenil (5 mu m), midazolam (1 mu m) did not diminish A delta-fiber evoked polysynaptic excitatory postsynaptic currents, suggesting that midazolam modulate the gamma-aminobutyric acid interneurons in the dorsal horn. Conclusions: Midazolam reduced excitatory synaptic transmission by acting on the gamma-aminobutyric acid type A/benzodiazepine receptor in interneurons, leading to a decrease in the excitability of spinal dorsal horn neurons. This may be a possible mechanism for the antinociception by midazolam in the spinal cord.
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