Dual MAP kinase pathways mediate opposing forms of long-term plasticity atCA3-CA1 synapses

Although the function of the p42/p44 mitogen-activated protein (MAP) kinase pathway in longterm 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 ki nase pathway, a parallel signaling cascade activated by distinct upstream k inases, mediates the induction of metabotropic glutamate receptor-dependent long-term depression at CA3-CA1 synapses. Thus, two parallel MAP kinase pa thways contribute to opposing forms of long-term plasticity at a central sy napse.