Dual MAP kinase pathways mediate opposing forms of long-term plasticity at CA3-CA1 synapses

V. Y. Bolshakov, L. Carboni, M. H. Cobb, S. A. Siegelbaum, F. Belardetti

Research output: Contribution to journalArticlepeer-review

204 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)1107-1112
Number of pages6
JournalNature neuroscience
Volume3
Issue number11
DOIs
StatePublished - 2000

ASJC Scopus subject areas

  • General Neuroscience

Fingerprint

Dive into the research topics of 'Dual MAP kinase pathways mediate opposing forms of long-term plasticity at CA3-CA1 synapses'. Together they form a unique fingerprint.

Cite this