| 8725598 |
Ishikawa T, Yaksh TL: [Concurrent characterization of spinal amino acid release and touch-evoked allodynia produced by spinal glycine or GABAA receptor antagonists]. Masui. 1996 Apr;45(4):439-44.
BACKGROUND: Previous work has shown that spinal strychinine (STR; glycine antagonist) or bicuculline (BIC; GABAA antagonist) yields a touch-evoked allodynia (TEA) that was blocked by NMDA receptor antagonists and that spinal NMDA receptor activation evokes glutamate release. In the present study, we examined the effects of spinal STR and BIC on TEA and the spinal release of amino acids, and spinal NMDA receptor activation with intrathecal NMDA. METHODS: In halothane-anesthetized (1.0%) Sprague-Dawley rats, TEA was assessed after intrathecal injection of STR (3 micrograms) or BIC (10 micrograms). TEA was scored as 0: no appearance to 3: strong agitation and was evaluated at 10-min intervals after injection of the drugs. Simultaneously, spinal release was monitored by using a microdialysis probe implanted into the lumbar subarachnoid space four days prior to the experiment. Glutamate (Glu) and taurine (Tau) in dialysates were measured by HPLC-UV. To assess the contribution of presynaptic glutaminergic neuron, the effects of intrathecal NMDA (3 micrograms) combined with either STR or BIC on spinal release were also examined. RESULTS: Time course of average TEA scores after intrathecal STR or BIC was similar at 10, 20 and 30 min (STR: 1.6, 0.3, 0; and, BIC: 1.8, 0.9, 0.1). Intrathecal BIC alone evoked a transient spinal release of Glu and Tau with increases by 54% and 68% respectively in the 0-10min samples while STR exerted no effect. Intrathecal NMDA faciliated the effects of BIC and STR on TEA score and spinal release of Glu and Tau. CONCLUSION: It is suggested that the development of allodynia may result from either a loss of GABAA inhibition on the presynaptic terminals and/or by a loss of postsynaptic glycine inhibition, the former facilitating spinal glutamate release, and the latter not. |
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