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Stress reverses plasticity in the pathway projecting from the ventromedial prefrontal cortex to the basolateral amygdala
Author(s) -
Maroun Mouna
Publication year - 2006
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.2006.05169.x
Subject(s) - ventromedial prefrontal cortex , basolateral amygdala , neuroscience , amygdala , psychology , prefrontal cortex , neuroplasticity , cognition
We have previously shown that high‐frequency stimulation to the basolateral amygdala (BLA) induces long‐term potentiation (LTP) in the ventromedial prefrontal cortex (vmPFC) and that prior exposure to inescapable stress inhibits the induction of LTP in this pathway [Maroun & Richter‐Levin (2003) J. Neurosci. , 23 , 4406–4409]. Here, we show that the reciprocal pathway projecting from the vmPFC to the BLA is resistant to the induction of LTP. Conversely, long‐term depression (LTD) is robustly induced in the BLA in response to low‐frequency stimulation to the vmPFC. Furthermore, prior exposure to inescapable stress reverses plasticity in this pathway, resulting in the promotion of LTP and the inhibition of LTD. Our findings suggest that, under normal and safe conditions, the vmPFC is unable to exert excitatory synaptic plasticity over the BLA; rather, LTD, which encodes memory of safety in the BLA, is favoured. Following stressful experiences, LTP in the BLA is promoted to encode memory of fear.