[Abstract Title]. - Society for Neuroscience

Program#/Poster#: 282.21/OO28
Topic: E.06.d. Cellular actions of stress
Title: Rapid effect of corticosterone in the amygdala
Authors: *H. KARST 1 , S. BERGER 2 , G. SCHÜTZ 2 , M. JOËLS 1 ;
1 SILS-CNS, Univ. of Amsterdam, Amsterdam, Netherlands; 2 German Cancer Res. Inst.,
Heidelberg, Germany
Abstract: In several brain structures e.g. the hypothalamus and the hippocampus, rapid effects of
corticosterone have been described. These effects are most likely mediated via membrane
located corticosteroid receptors. We reported a rapid increase by corticosterone of miniature
EPSC frequency via mineralocorticoid receptors located on the membrane (mMRs) of
hippocampal CA1 neurons (PNAS, 2005, 102, 19204).The receptors that are responsible for this
effect appear to have the same genetic origin as the nuclear receptors, but have a 10 fold lower
affinity for corticosterone. Therefore in contrast to the nuclear MRs, which are already activated
with basal corticosterone levels, the mMRs might affect excitability of CA1 neurons only during
periods of stress. The mMRs are located presynaptically and upon activation cause an increase in
the release of glutamate via the MEK-ERK1/2 pathway.
Another limbic structure that is in involved in stress related behavior is the amygdala. Especially
memory consolidation of emotionally salient events depends on this structure. Recently,
membrane located glucocorticoid receptors were demonstrated in the amygdala (Neuroscience,
2005, 136, 289). In the current study we investigated a possible rapid modulation by
corticosterone of the spontaneous mEPSCs in two substructures of the amygdala, the basolateral
amygdala (BLA) and the central amygdala (CeA). In the CeA there was no rapid effect of
corticosterone, neither on the frequency nor on the mean amplitude of the mEPSCs. However, in
the BLA, application of 100 nM corticosterone induced an increase in the frequency within 10
minutes. The mean amplitude of the mEPSCs was not affected by corticosterone. In contrast to
the hippocampus the effect in the BLA was not reversible, indicating that rapid effects might
develop into long term effects. In inducible neuron-specific GR knockout mice the rapid effect
persisted. However in inducible neuron-specific MR knockout mice, the rapid effect was entirely
absent. The data suggests that in the BLA too corticosterone affects the glutamate release
probability via the MRs. However, in the BLA these effects seem to be far more persistent. This
could mean that stressors involving activation of the amygdala have a more lasting impact. We
are currently investigating the possible mechanism underlying the long lasting effect of
corticosterone on the mEPSC frequency.
Disclosures: H. Karst, None; S. Berger, None; G. Schütz, None; M. Joëls, None.
Poster
282. Stress and the Brain: Cellular Actions of Stress