Abstract
The amygdala is considered central in mediating stress-related changes of hippocampal functions. However, it remains unclear whether different amygdala subnuclei have different roles in coordinating stress effects. Here, we report that stress exposure caused an immediate increase of extracellular signal-regulated kinase (ERK)1/2 phosphorylation in the hippocampal area CA1 and the basolateral amygdala (BLA) and after a delay in the central amygdala (CEA). Exposure to the novel environment following stress increased ERK1/2 phosphorylation in the CEA, but reversed the stress-induced increase of ERK1/2 phosphorylation in the hippocampal area CA1 and the BLA. Either ERK1/2 inhibitor U0126 or N-methyl-D-aspartate (NMDA) receptor antagonist DL-(-)-2-amino-5- phosphonopentanoic acid (APV) administration into the BLA, but not the CEA, blocked the stress effects on hippocampal long-term potentiation (LTP) and long-term depression. Novelty-exploration-induced reversal of stress effects was prevented when animals were injected U0126 or APV into the CEA, but not the BLA, before subjected to the novel environment. The ability of novelty exploration to reverse the stress effects was mimicked by intra-CEA infusion of NMDA. These findings suggest that BLA ERK1/2 signaling pathway is critical to mediate the stress effects on hippocampal synaptic plasticity; the activation of CEA ERK1/2, in contrast, appears to mediate the reversal of Stress effects.
| Original language | English |
|---|---|
| Pages (from-to) | 548-563 |
| Number of pages | 16 |
| Journal | Hippocampus |
| Volume | 18 |
| Issue number | 6 |
| DOIs | |
| Publication status | Published - 2008 |
| Externally published | Yes |
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Keywords
- Amygadala
- Hippocampus
- Long-term depression
- Long-term potentiation
- Stress
ASJC Scopus subject areas
- Neuroscience(all)
Cite this
Differential roles of basolateral and central amygdala on the effects of uncontrollable stress on hippocampal synaptic plasticity. / Yang, Chih Hao; Huang, Chiung Chun; Hsu, Kuei Sen.
In: Hippocampus, Vol. 18, No. 6, 2008, p. 548-563.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Differential roles of basolateral and central amygdala on the effects of uncontrollable stress on hippocampal synaptic plasticity
AU - Yang, Chih Hao
AU - Huang, Chiung Chun
AU - Hsu, Kuei Sen
PY - 2008
Y1 - 2008
N2 - The amygdala is considered central in mediating stress-related changes of hippocampal functions. However, it remains unclear whether different amygdala subnuclei have different roles in coordinating stress effects. Here, we report that stress exposure caused an immediate increase of extracellular signal-regulated kinase (ERK)1/2 phosphorylation in the hippocampal area CA1 and the basolateral amygdala (BLA) and after a delay in the central amygdala (CEA). Exposure to the novel environment following stress increased ERK1/2 phosphorylation in the CEA, but reversed the stress-induced increase of ERK1/2 phosphorylation in the hippocampal area CA1 and the BLA. Either ERK1/2 inhibitor U0126 or N-methyl-D-aspartate (NMDA) receptor antagonist DL-(-)-2-amino-5- phosphonopentanoic acid (APV) administration into the BLA, but not the CEA, blocked the stress effects on hippocampal long-term potentiation (LTP) and long-term depression. Novelty-exploration-induced reversal of stress effects was prevented when animals were injected U0126 or APV into the CEA, but not the BLA, before subjected to the novel environment. The ability of novelty exploration to reverse the stress effects was mimicked by intra-CEA infusion of NMDA. These findings suggest that BLA ERK1/2 signaling pathway is critical to mediate the stress effects on hippocampal synaptic plasticity; the activation of CEA ERK1/2, in contrast, appears to mediate the reversal of Stress effects.
AB - The amygdala is considered central in mediating stress-related changes of hippocampal functions. However, it remains unclear whether different amygdala subnuclei have different roles in coordinating stress effects. Here, we report that stress exposure caused an immediate increase of extracellular signal-regulated kinase (ERK)1/2 phosphorylation in the hippocampal area CA1 and the basolateral amygdala (BLA) and after a delay in the central amygdala (CEA). Exposure to the novel environment following stress increased ERK1/2 phosphorylation in the CEA, but reversed the stress-induced increase of ERK1/2 phosphorylation in the hippocampal area CA1 and the BLA. Either ERK1/2 inhibitor U0126 or N-methyl-D-aspartate (NMDA) receptor antagonist DL-(-)-2-amino-5- phosphonopentanoic acid (APV) administration into the BLA, but not the CEA, blocked the stress effects on hippocampal long-term potentiation (LTP) and long-term depression. Novelty-exploration-induced reversal of stress effects was prevented when animals were injected U0126 or APV into the CEA, but not the BLA, before subjected to the novel environment. The ability of novelty exploration to reverse the stress effects was mimicked by intra-CEA infusion of NMDA. These findings suggest that BLA ERK1/2 signaling pathway is critical to mediate the stress effects on hippocampal synaptic plasticity; the activation of CEA ERK1/2, in contrast, appears to mediate the reversal of Stress effects.
KW - Amygadala
KW - Hippocampus
KW - Long-term depression
KW - Long-term potentiation
KW - Stress
UR - http://www.scopus.com/inward/record.url?scp=45149116038&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=45149116038&partnerID=8YFLogxK
U2 - 10.1002/hipo.20414
DO - 10.1002/hipo.20414
M3 - Article
C2 - 18306298
AN - SCOPUS:45149116038
VL - 18
SP - 548
EP - 563
JO - Hippocampus
JF - Hippocampus
SN - 1050-9631
IS - 6
ER -