Qian Z, Gilbert M, Kandel E R
Howard Hughes Medical Institute, College of Physicians and Surgeons of Columbia University, New York, New York 10032, USA.
Learn Mem. 1994 Sep-Oct;1(3):180-8.
Recent studies indicate that stimulation of NMDA receptors in cultured hippocampal cells activates MAP kinase. Although the pathway whereby MAP kinase is activated has been been characterized, little is known about the mechanisms that shut off MAP kinase. In the course of analyzing several immediate-early genes identified previously by differential screen as inducible by seizure activity, we found that one of them, BAD2, encodes dual purpose, threonine/tyrosine phosphates with specific activity directed against MAP kinase (MKP-1). In situ hybridization of BAD2 demonstrates that stimuli that produce seizure, kindling, and long-term potentiation cause a rapid increase in BAD2 mRNA (within 0.5-1 hr after stimulation) that has, in each case, a distinctive pattern of expression in the brain. In these regions, the induction of a MAP kinase-specific phosphatase may provide a negative feedback control associated with long-term synaptic changes.
最近的研究表明，在培养的海马细胞中刺激NMDA受体可激活丝裂原活化蛋白激酶（MAP激酶）。尽管MAP激酶被激活的途径已得到表征，但对于关闭MAP激酶的机制却知之甚少。在分析先前通过差异筛选确定为可被癫痫发作活动诱导的几个立即早期基因的过程中，我们发现其中一个基因BAD2编码具有针对MAP激酶（MKP-1）的特定活性的双功能苏氨酸/酪氨酸磷酸酶。BAD2的原位杂交表明，产生癫痫发作、点燃和长时程增强的刺激会导致BAD2 mRNA迅速增加（刺激后0.5 - 1小时内），并且在每种情况下，在大脑中都有独特的表达模式。在这些区域，MAP激酶特异性磷酸酶的诱导可能提供与长期突触变化相关的负反馈控制。
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