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Pharmacological modulation of brain levels of glutamate and GABA in rats exposed to total sleep deprivation

机译:完全睡眠剥夺大鼠脑中谷氨酸和GABA水平的药理调节

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摘要

Modulation of gamma-aminobutyric acid (GABA) and glutamate by selected antidepressants and anticonvulsants could play a beneficial role in total sleep deprivation (TSD) caused by depressed mood. In the present study, albino rats were exposed to TSD for five days. On the sixth day, the brains were removed, and GABA and glutamate levels were measured in the prefrontal cortex and thalamus to identify TSD-induced changes in untreated rats and in rats treated with carbamazepine 40 mg/kg intraperitoneally (IP), fluoxetine 20 mg/kg IP, or desipramine 10 mg/kg IP. Carbamazepine and fluoxetine significantly increased GABA and reduced glutamate levels in both brain areas. Desipramine administration did not affect GABA or glutamate concentrations in the tested brain areas; levels were comparable with those induced by TSD without treatment. These results suggest that administration of carbamazepine or fluoxetine could have a beneficial effect by increasing GABA levels during TSD.
机译:选定的抗抑郁药和抗惊厥药对γ-氨基丁酸(GABA)和谷氨酸的调节可在情绪低落引起的总睡眠不足(TSD)中发挥有益作用。在本研究中,白化病大鼠暴露于TSD 5天。在第六天,移开大脑,测量额叶前额叶和丘脑中的GABA和谷氨酸水平,以鉴定TSD诱导的未治疗大鼠和经卡马西平40 mg / kg腹膜内(IP),氟西汀20 mg治疗的大鼠的变化/ kg IP,或地昔帕明10 mg / kg IP。卡马西平和氟西汀可显着增加两个脑区的GABA并降低谷氨酸水平。地西拉明的给药对被测脑区的GABA或谷氨酸浓度没有影响。该水平与未经治疗的TSD诱导的水平相当。这些结果表明,卡马西平或氟西汀的给药可通过在TSD期间增加GABA的水平来产生有益的作用。

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