Impaired long-term potentiation in c-Jun N-terminal kinase 2-deficient mice

J Neurochem. 2005 Apr;93(2):463-73. doi: 10.1111/j.1471-4159.2005.03037.x.

Abstract

c-Jun N-terminal kinases (JNKs) are thought to be involved in regulating synaptic plasticity. We therefore investigated the specific role of JNK2 in modulating long-term potentiation (LTP) in hippocampus during development, using JNK2-deficient mice. The morphological structure and the numbers of both NeuN, a specific neuronal marker, and GABA-positive neurons in the hippocampal areas were similar in wild-type and Jnk2(-/-) mice. Western blot analysis revealed that JNK2 expression was higher and stable at 1 and 3 months of age, but JNK1 levels were lower at 1 month of age and almost undetectable in 3-month-old wild-type mice. In contrast to wild-type mice, there was a significant increase in JNK1 expression in JNK2 mutant mice, especially at 1 month of age. Electrophysiological studies demonstrated that LTP was impaired in both the CA1 and CA3 regions in 1-month-old, but not in adult, Jnk2(-/-) mice, probably owing to decreased presynaptic neurotransmitter release. Moreover, late-phase LTP, but not early-phase LTP, was impaired in the Jnk2(-/-) adult mice, suggesting that JNK2 plays a role in transforming early LTP to late LTP. Together, the data highlight the specific role of JNK2 in hippocampal synaptic plasticity during development.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Excitatory Postsynaptic Potentials / genetics
  • Hippocampus / enzymology
  • Long-Term Potentiation / genetics*
  • Mice
  • Mice, Knockout
  • Mitogen-Activated Protein Kinase 9 / biosynthesis
  • Mitogen-Activated Protein Kinase 9 / deficiency*
  • Mitogen-Activated Protein Kinase 9 / genetics*
  • Neuronal Plasticity / genetics*

Substances

  • Mitogen-Activated Protein Kinase 9