The Effect of Intrathecal NMDA and non-NMDA Receptor Antagonist on the Hyperalgesia Observed after Thermal Injury in the Rat / 대한마취과학회지

BACKGROUND: Previous reports have described NMDA antagonist reduced the nerve injury induced or inflammatory thermal hyperalgesia. This study evaluated the effects of spinally administered excitatory amino acid antagonists on the thermal hyperalgesia state induced by mild burn. METHODS: The measured response was the latency to paw withdrawal of each hindpaw after application of a focused heat lamp on the plantar surface of the paw through a glass plate upon which the animal stood. In this work, MK801, non-competitive NMDA receptor antagonist, AP5, competitive NMDA receptor antagonist, CNQX, non-NMDA receptor antagonist were injected through chronically implanted lumbar intrathecal catheters in rats with mild burn injury on the right hindpaw. RESULTS: In the normal left hindpaw, MK801, AP5 and CNQX had little effect upon paw withdrawal latency (PWL) at intrathecal doses which do not produce readily detectable motor weakness. In the right hyperalgesic hindpaw, AP5 significantly reduced PWL at a dose-dependent fashion, MK801 reduced PWL to some extent, and CNQX did not reduced PWL. CONCLUSIONS: These results suggested that spinal NMDA receptors play an important role in the hyperalgesia induced by mild burn injury.

Effects of intracere broventri cular injection of L-proline on learning and memory in mice / 中国药理学通报

In step-down tests in mice,the effects of L -proline 0.1 - 100?g ? mouse-1 icv on memory acquisition were not observed, but L -proline0. l~10?g ? mouse-1 icv could significantly improve the anisodine- induced impairments of memory acquisition. This effect of L-proline 1?g ? mouse-1 icv could not be antagonized with D-2-amino-5-phosphonovaleric acid(APS), the N-methyl-D-aspartate (NMDA) receptor antagonist. L-proline 1?g ? mouse-1 icv could also improve memory acquisition impairment induced by high GABA level in brain. This results suggested that L - proline may improve the memory as the modulator or possibly through GABA.