Bolshakov V Y, Carboni L, Cobb M H, Siegelbaum S A, Belardetti F
McLean Hospital, Department of Psychiatry, Harvard Medical School, 115 Mill Street, Belmont, Massachusetts 02478, USA.
Nat Neurosci. 2000 Nov;3(11):1107-12. doi: 10.1038/80624.
Although the function of the p42/p44 mitogen-activated protein (MAP) kinase pathway in long-term potentiation at hippocampal CA3-CA1 synapses has been well described, relatively little is known about the importance of the p38 MAP kinase pathway in synaptic plasticity. Here we show that the p38 MAP kinase pathway, a parallel signaling cascade activated by distinct upstream kinases, mediates the induction of metabotropic glutamate receptor-dependent long-term depression at CA3-CA1 synapses. Thus, two parallel MAP kinase pathways contribute to opposing forms of long-term plasticity at a central synapse.
尽管p42/p44丝裂原活化蛋白（MAP）激酶通路在海马CA3-CA1突触的长时程增强中的作用已得到充分描述，但关于p38 MAP激酶通路在突触可塑性中的重要性却知之甚少。我们在此表明，p38 MAP激酶通路是由不同上游激酶激活的平行信号级联反应，它介导了CA3-CA1突触处代谢型谷氨酸受体依赖性长时程抑制的诱导。因此，两条平行的MAP激酶通路在中枢突触处促成了相反形式的长时程可塑性。
