Sharma S K, Bolster B, Dakshinamurti K
Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Manitoba, Winnipeg.
J Neurol Sci. 1994 Jan;121(1):1-9. doi: 10.1016/0022-510x(94)90148-1.
Computerized electroencephalography and thalamic ventro-posterior lateral (VPL) unit activities were recorded from pyridoxine-deficient and pair-fed pyridoxine-supplemented adult male rats. Pyridoxine-deficient animals exhibited slow electroencephalograms (EEG) represented by the dominance of delta activity and reduced seizure thresholds to local (VPL) application of either picrotoxin or pentylene tetrazole. Frequency and amplitude of thalamic VPL unit activity were significantly reduced in pyridoxine-deficient rats as compared to pyridoxine-supplemented controls. Pyridoxine-deficient rats exhibited irregular unit activity with frequent bursts and electrosilent periods in response to local (VPL) picrotoxin or pentylene tetrazole microinjections. They also exhibited severe seizure discharge activity of prolonged duration at any given dose of either picrotoxin or pentylene tetrazole. This was represented by significantly increased burst frequency, burst duration and reduced seizure latencies. Unit activity was transformed into burst discharge activity with intermittent electrosilent zones during picrotoxin or pentylene tetrazole epileptogenesis. Cerebral gamma aminobutyric acid (GABA) level was reduced and glutamate concentration increased in pyridoxine-deficient rats when compared with pyridoxine-supplemented controls. Local (VPL) microinjection of GABA or pyridoxine induced neuronal recovery in both convulsant-treated normal and pyridoxine-deficient rats. Neuronal recovery was however delayed in pyridoxine-deficient rats. Neuronal recovery was associated with a significant increase in EEG background frequency and reduction in delta frequencies in the EEG records of both normal and pyridoxine-deficient rats. Reduced seizure threshold and delayed neuronal recovery are related to the significantly reduced brain regional GABA and elevated glutamate levels in pyridoxine-deficient rats.
对成年雄性吡哆醇缺乏大鼠和配对喂养的吡哆醇补充大鼠进行了计算机化脑电图和丘脑腹后外侧（VPL）单位活动记录。吡哆醇缺乏的动物表现出以δ活动为主导的慢脑电图（EEG），并且对局部（VPL）应用苦味毒或戊四氮的癫痫发作阈值降低。与补充吡哆醇的对照组相比，吡哆醇缺乏大鼠丘脑VPL单位活动的频率和幅度显著降低。吡哆醇缺乏大鼠在局部（VPL）注射苦味毒或戊四氮后表现出不规则的单位活动，伴有频繁的爆发和电静息期。在任何给定剂量的苦味毒或戊四氮下，它们还表现出持续时间延长的严重癫痫放电活动。这表现为爆发频率显著增加、爆发持续时间延长和癫痫发作潜伏期缩短。在苦味毒或戊四氮致痫过程中，单位活动转变为伴有间歇性电静息区的爆发放电活动。与补充吡哆醇的对照组相比，吡哆醇缺乏大鼠脑内γ-氨基丁酸（GABA）水平降低，谷氨酸浓度升高。在惊厥处理的正常大鼠和吡哆醇缺乏大鼠中，局部（VPL）注射GABA或吡哆醇均可诱导神经元恢复。然而，吡哆醇缺乏大鼠的神经元恢复延迟。神经元恢复与正常大鼠和吡哆醇缺乏大鼠脑电图记录中EEG背景频率显著增加和δ频率降低有关。癫痫发作阈值降低和神经元恢复延迟与吡哆醇缺乏大鼠脑区GABA显著降低和谷氨酸水平升高有关。
