Protein Tau is a very unequal phosphoric microtubule associated protein, which affect the transport of substances in the axons of the neurons, whose phosphorylation is one of the key methods to regulate neuronal function. The hyperphosphorylation of protein Tau can damage the learning and memory of rats. The impairment of learning-memory induced by electroconvulsive shock in depressed rats is relevant to the function failure of glutamic acid signal system. The phosphorylation of protein Tau can be up-regulated by the individual stress level through the excitatory neurotransmission system. The mechanisms of 2, 6-diisopropylphenol effect on the central nerve system relate to inhibiting the release of glutamic acid and the activity of NMDAR. And the 2, 6-diisopropylphenol can protects against the impairment of learning-memory induced by electroconvulsive shock in depressed rats though inhibiting the excitotoxicty of glutamate. The rise of glutamic acid which induced by electroconvulsive shock in depressed rats can lead to the impairment of learning-memory through up-regulating the hyperphosphorylation of protein Tau? The 2, 6-diisopropylphenol can protect against this process? This study explore the reversion of the 2, 6-diisopropylphenol against the impairment of learning-memory and the hyperphosphorylation of protein Tau induced by electroconvulsive shock in depressed rats, in order to provide experimental evidence for neuropsychological mechanisms on improving learning and memory and the clinical intervention treatment. According to the design of factorial analysis, two intervention factors were set up: the electroconvulsive shock (two levels: no disposition; a course of electroconvulsive shock) and the 2, 6- diisopropylphenol (two levels: 5 ml Saline was injected peritoneally; 5 ml 2, 6-diisopropylphenol was injected peritoneally by dosage of 100 mg/kg). Thirty-two adult depression model rats whose olfactory bulbs were removed were randomly divided into four experimental groups (n=8, in each group): group Ⅰ(5 ml 2, 6-diisopropylphenol was injected peritoneally in the Sprague-Dawley rats by dosage of 100 mg/kg); group Ⅱ(5 ml 2, 6- diisopropylphenol was injected peritoneally in the Sprague-Dawley rats by dosage of 100 mg/kg and giving a course of electroconvulsive shock); group Ⅲ(5ml Saline was injected peritoneally in the Sprague-Dawley rats); group Ⅳ(5 ml saline was injected peritoneally in the Sprague-Dawley rats and giving a course of electroconvulsive shock). The Morris water maze test started within 1 day after the course of electroconvulsive shock finished in order to evaluate learning-memory. The hippocampus was removed from rats within 1 day after the Morris water maze test finished. The content of glutamate in the hippocampus of rats was detected by high performance liquid chromatography. The content of Protein Tau which includes Tau-5 (Total protein Tau), p-PHF1^Ser396/404, p-AT8^Ser199/202, p-12E8^Ser262, GSK-3β^1H8 and PP-2A in the hippocampus of rats was detected with Western blotting. The electroconvulsive shock and the 2, 6-diisopropylphenol can induce the impairment of learning-memory in depressed rats, extending the evasive latency time and shortening the space exploration time. And both influences present subtract effect. The electroconvulsive shock can significantly up-regulate the content of glutamate in the hippocampus of depressed rats which was reduced by 2, 6-diisopropylphenol. And both influences present subtract effect. The electroconvulsive shock and the 2, 6-diisopropylphenol does not affect the total protein Tau and protein PP-2A in the hippocampus of rats. The electroconvulsive shock can up-regulate the hyperphosphorylation of protein Tau and the expression of GSK-3β^1H8 in the hippocampus of depressed rats, which is reduced by 2, 6- diisopropylphenol. And both influences present subtract effect. Our results indicate that the electroconvulsive shock up-regulates the content of glutamate in the hippocampus of depressed rats, which up-regulates the hyperphosphorylation of protein Tau through up-regulating the expression of GSK-3β^1H8, and further induce the impairment of learning-memory in depressed rats. Wheareas, the 2, 6-diisopropylphenol protects against the impairment of learning-memory and reduce the hyperphosphorylation of protein Tau induced by electroconvulsive shock in depressed rats through reducing the expression of GSK-3β^1H8 and the content of glutamate in the hippocampus.