Role of MAP kinase in neurons

Kohji Fukunaga, Eishichi Miyamoto

Research output: Contribution to journalArticlepeer-review

228 Citations (Scopus)

Abstract

Extracellular stimuli such as neurotransmitters, neurotrophins, and growth factors in the brain regulate critical cellular events, including synaptic transmission, neuronal plasticity, morphological differentiation and survival. Although many such stimuli trigger Ser/Thr-kinase and tyrosine- kinase cascades, the extracellular signal-regulated kinases, ERK1 and ERK2, prototypic members of the mitogen-activated protein (MAP) kinase family, are most attractive candidates among protein kinases that mediate morphological differentiation and promote survival in neurons. ERK1 and ERK2 are abundant in the central nervous system (CNS) and are activated during various physiological and pathological events such as brain ischemia and epilepsy. In cultured hippocampal neurons, simulation of glutamate receptors can activate ERK signaling, for which elevation of intracellular Ca2+ is required. In addition, brain-derived neurotrophic factor and growth factors also induce the ERK signaling and here, receptor-coupled tyrosine kinase activation has an association. We describe herein intracellular cascades of ERK signaling through neurotransmitters and neurotrophic factors. Putative functional implications of ERK and other MAP-kinase family members in the central nervous system are give attention.

Original languageEnglish
Pages (from-to)79-95
Number of pages17
JournalMolecular Neurobiology
Volume16
Issue number1
DOIs
Publication statusPublished - 1998 Jan 1
Externally publishedYes

Keywords

  • Apoptosis
  • BDNF
  • Calmodulin-dependent protein kinase
  • Central nervous system
  • Glutamate receptor
  • Hippocampus
  • MAP kinase
  • Stress-activated protein kinase
  • Synaptic plasticity

ASJC Scopus subject areas

  • Neurology
  • Cellular and Molecular Neuroscience

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