TY - JOUR
T1 - Bidirectional modulation of hippocampal long-term potentiation under stress and no-stress conditions in basolateral amygdala-lesioned and intact rats
AU - Korz, Volker
AU - Frey, Julietta U.
PY - 2005/8/10
Y1 - 2005/8/10
N2 - Hippocampal long-term potentiation (LTP) is widely considered as a cellular model for learning and memory formation. We have shown previously that protein synthesis-independent, early dentate gyrus (DG) LTP, lasting ∼4-5 h, can be transformed into a late-LTP with a duration of ≥24 h by a brief acute swim stress experience (high-stress condition). This reinforcement requires the activation of mineralocorticoid receptors and protein synthesis. The basolateral amygdala (BLA) is known to modulate glucocorticoid effects on the consolidation of spatial/contextual memory via a β-adrenergic mechanism. Interestingly, hippocampal DG-LTP can also be indirectly modulated by β-adrenergic and cholinergic/muscarinergic processes. Here, we show that the reinforcement of early-DG-LTP under high-stress conditions depends on the processing of novel spatial/contextual information. Furthermore, this reinforcement was blocked in BLA-lesioned animals compared with sham-operated and intact controls; however, it was not dependent on β-adrenergic or cholinergic/muscarinergic receptor activation. In contrast, under low-stress conditions, the induction of late-LTP in BLA-lesioned animals is facilitated, and this facilitation, again, was dependent on β-adrenergic activation. The data suggest that DG-LTP maintenance can be influenced by the BLA through different mechanisms: a short-lasting corticosterone-dependent and β-adrenergic-independent mechanism and a long-lasting mechanism that facilitated hippocampal β-adrenergic mechanisms.
AB - Hippocampal long-term potentiation (LTP) is widely considered as a cellular model for learning and memory formation. We have shown previously that protein synthesis-independent, early dentate gyrus (DG) LTP, lasting ∼4-5 h, can be transformed into a late-LTP with a duration of ≥24 h by a brief acute swim stress experience (high-stress condition). This reinforcement requires the activation of mineralocorticoid receptors and protein synthesis. The basolateral amygdala (BLA) is known to modulate glucocorticoid effects on the consolidation of spatial/contextual memory via a β-adrenergic mechanism. Interestingly, hippocampal DG-LTP can also be indirectly modulated by β-adrenergic and cholinergic/muscarinergic processes. Here, we show that the reinforcement of early-DG-LTP under high-stress conditions depends on the processing of novel spatial/contextual information. Furthermore, this reinforcement was blocked in BLA-lesioned animals compared with sham-operated and intact controls; however, it was not dependent on β-adrenergic or cholinergic/muscarinergic receptor activation. In contrast, under low-stress conditions, the induction of late-LTP in BLA-lesioned animals is facilitated, and this facilitation, again, was dependent on β-adrenergic activation. The data suggest that DG-LTP maintenance can be influenced by the BLA through different mechanisms: a short-lasting corticosterone-dependent and β-adrenergic-independent mechanism and a long-lasting mechanism that facilitated hippocampal β-adrenergic mechanisms.
KW - Basolateral amygdala
KW - Early-LTP
KW - Late-LTP
KW - Locus ceruleus
KW - Memory
KW - Stress
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UR - http://www.scopus.com/inward/citedby.url?scp=23744469219&partnerID=8YFLogxK
U2 - 10.1523/JNEUROSCI.0910-05.2005
DO - 10.1523/JNEUROSCI.0910-05.2005
M3 - Article
C2 - 16093390
AN - SCOPUS:23744469219
SN - 0270-6474
VL - 25
SP - 7393
EP - 7400
JO - Journal of Neuroscience
JF - Journal of Neuroscience
IS - 32
ER -