Differential patterns of extracellular signal-regulated kinase-1 and-2 phosphorylation in rat limbic brain regions after short-term and long-term inhibitory avoidance learning
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作者:
Chai, SC
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机构:Fu Jen Catholic Univ, Sch Med, Taipei 24205, Taiwan
Chai, SC
Holahan, MR
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机构:Fu Jen Catholic Univ, Sch Med, Taipei 24205, Taiwan
Holahan, MR
Shyu, BC
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机构:Fu Jen Catholic Univ, Sch Med, Taipei 24205, Taiwan
Shyu, BC
Wang, CC
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机构:Fu Jen Catholic Univ, Sch Med, Taipei 24205, Taiwan
Wang, CC
机构:
[1] Fu Jen Catholic Univ, Sch Med, Taipei 24205, Taiwan
[2] Chung Shan Med Univ, Dept Psychol, Taichung, Taiwan
[3] Northwestern Univ, Dept Psychol, Evanston, IL USA
Activation of the extracellular signal-regulated kinase-11 and -2 has been shown to be required for neural plasticity and memory. Previous pharmacological studies have demonstrated that inhibition of extracellular signal-regulated kinase-1 and -2 blocks inhibitory avoidance retention. The aim of the present study was to investigate the different neural substrates underlying short- and long-term inhibitory avoidance learning and memory in rats using phosphorylated extracellular signal-regulated kinase-1 and -2 labeling as an index of plasticity. Short- and long-term retention tests were given 10 min or 24 h after inhibitory avoidance training. A significant elevation in the number of phosphorylated extracellular signal-regulated kinase-11 and -2-immunoreactive neurons was observed in area 1 of anterior cingulate cortex, the secondary motor cortex, lateral orbital cortex, claustrum, and the medial amygdala nucleus after the short-term inhibitory avoidance test. After the long-term retention test, phosphorylated extracellular signal-regulated kinase-1 and -2-immunoreactive neurons were localized in area 1 of anterior cingulate cortex, prelimbic cortex, and the central nucleus of amygdala. This suggests that phosphorylated extracellular signal-regulated kinase-1 and -2-immunoreactivity may reveal different brain regions involved in the storage of short- and long-term aversive memories. (c) 2005 Published by Elsevier Ltd on behalf of IBRO.