Gamaro Giovana D, Streck Emilio L, Matté Cristiane, Prediger Martha E, Wyse Angela T S, Dalmaz Carla
Departamento de Bioquimica, ICBS, Universidade Federal do Rio Grande do Sul, Rua Ramiro Barcelos 2600-Anexo. CEP: 90035-003. Porto Alegre, RS, Brazil.
Neurochem Res. 2003 Sep;28(9):1339-44. doi: 10.1023/a:1024988113978.
The effect of a model of depression using female rats on Na+, K+-ATPase activity in hippocampal synaptic plasma membranes was studied. In addition, the effect of further chronic treatment with fluoxetine on this enzyme activity was verified. Sweet food consumption was measured to evaluate the efficacy of this model in inducing a state of reduced response to rewarding stimili. After 40 days of mild stress, a reduction in sweet food ingestion was observed. Reduction of hippocampal Na+, K+-ATPase activity was also observed. Treatment with fluoxetine increased this enzyme activity and reversed the effect of stress. Chronic fluoxetine decreased the ingestion of sweet food in both groups. This result is in agreement with suggestions that reduction of Na+, K+-ATPase activity is a caracteristic of depressive disorders. Fluoxetine reversed this effect. Therefore it is possible that altered Na+, K+-ATPase activity may be involved in the pathophysiology of depression in patients.
研究了使用雌性大鼠的抑郁症模型对海马突触质膜中钠钾ATP酶活性的影响。此外，还验证了用氟西汀进一步长期治疗对该酶活性的影响。通过测量甜食消耗量来评估该模型在诱导对奖励刺激反应降低状态方面的功效。经过40天的轻度应激后，观察到甜食摄入量减少。还观察到海马钠钾ATP酶活性降低。用氟西汀治疗可增加该酶活性并逆转应激的影响。长期使用氟西汀会使两组的甜食摄入量减少。这一结果与钠钾ATP酶活性降低是抑郁症特征的观点一致。氟西汀逆转了这一效应。因此，钠钾ATP酶活性改变可能参与了患者抑郁症的病理生理学过程。
