Mice lacking the ERK1 isoform of MAP kinase are unimpaired in emotional learning

Citation
Jc. Selcher et al., Mice lacking the ERK1 isoform of MAP kinase are unimpaired in emotional learning, LEARN MEM, 8(1), 2001, pp. 11-19
Citations number
33
Categorie Soggetti
Neurosciences & Behavoir
Journal title
LEARNING & MEMORY
ISSN journal
10720502 → ACNP
Volume
8
Issue
1
Year of publication
2001
Pages
11 - 19
Database
ISI
SICI code
1072-0502(200101/02)8:1<11:MLTEIO>2.0.ZU;2-M
Abstract
The extracellular signal-regulated kinases (ERKs) are members of the mitoge n-activated protein kinase (MAPK) superfamily of enzymes and have recently garnered considerable attention in the field of learning and memory. ERK ac tivation has been shown to be required for the induction of long-term poten tiation (LTP) in the rat hippocampus and for the formation of associative a nd spatial memories in both the rat and the mouse. However, the individual roles for the two isoforms of ERK have yet to be deciphered. To investigate the specific contribution of the ERK1 (p44) isoform of MAPK to mammalian l earning, we performed a general behavioral and physiological characterizati on of mice lacking the ERK1 gene. The ERK1-null animals demonstrated signif icantly higher levels of activity in the open field test. However, we obser ved no other discernible deficits in the ERK1 knockout mice in our behavior al testing. Specifically, no differences were observed in the acquisition o r retention (24 h and 2 wk after training) of either contextual or cue fear conditioning between the ERK1(-/-) and their wild-type littermate controls . In addition, no learning phenotype was observed in the passive avoidance test. When hippocampal slices were analyzed, we found no deficits in baseli ne synaptic transmission or in tetanus-induced LTP in hippocampal area CA1. We found no apparent compensatory changes in the expression of ERK2 (p42 M APK). We conclude that hippocampus and amygdala-dependent emotional learnin g does not depend critically on the activity of ERK1.