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Action of Isoflurane on the Substantia Gelatinosa Neurons of the Adult Rat Spinal Cord
Authors:Wakai, Ayako M.D.   Kohno, Tatsuro M.D., Ph.D.&#x     Yamakura, Tomohiro M.D., Ph.D.&#x     Okamoto, Manabu M.D., Ph.D.&#x     Ataka, Toyofumi M.D., Ph.D.&#x     Baba, Hiroshi M.D., Ph.D.   
Affiliation:Wakai, Ayako M.D.*; Kohno, Tatsuro M.D., Ph.D.†; Yamakura, Tomohiro M.D., Ph.D.‡; Okamoto, Manabu M.D., Ph.D.†; Ataka, Toyofumi M.D., Ph.D.†; Baba, Hiroshi M.D., Ph.D.§
Abstract:Background: Although isoflurane, a volatile anesthetic, can block the motor response to noxious stimulation (immobility and analgesia) and suppress autonomic responsiveness, how it exerts these effects at the neuronal level in the spinal cord is not fully understood.

Methods: The effects of a clinically relevant concentration (1 rat minimum alveolar concentration [MAC]) of isoflurane on electrically evoked and spontaneous excitatory/inhibitory transmission and on the response to exogenous administration of the [gamma]-aminobutyric acid type A receptor agonist muscimol were examined in lamina II neurons of adult rat spinal cord slices using the whole cell patch clamp technique. The effect of isoflurane on the action potential-generating membrane property was also examined.

Results: Bath-applied isoflurane (1.5%, 1 rat MAC) diminished dorsal root-evoked polysynaptic but not monosynaptic excitatory postsynaptic currents. Glutamatergic miniature excitatory postsynaptic currents were also unaffected by isoflurane. In contrast, isoflurane prolonged the decay phase of evoked and miniature [gamma]-aminobutyric acid type A receptor-mediated inhibitory postsynaptic currents and increased the amplitude of the muscimol-induced current. Isoflurane had little effect on action potential discharge activity.

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