Biology Reference
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protein (CREBA133), show unaltered expression of LTP and depotentiation in the BLA
(Rammes et al. 2000). In Figure 2 the above discussed mechanisms of LA-LTP and LA-LTD
are schematically summarized.
Recent results suggest that calcium influx through NMDA receptors and VDCCs during
fear conditioning activates PKA and CaMK IV resulting in CREB phosphorylation. The
phosphorylated CREB binds to BDNF promoter and up-regulates the expression of BDNF in
the amygdala, which helps the consolidation of fear memory (Ou and Gean 2007). BDNF acts
through the high-affinity receptor trkB. This receptor is highly expressed in the amygdala
(Krause et al. 2007)
and activation of trkB trough BDNF has been shown to induce a specific
form of LTP, at least in the hippocampus (Bramham and Messaoudi 2005) Thus, a link
between synaptic plasticity and BDNF may exist also on the level of the amygdala. Along
this line, it has been shown that expression of conditioned fear is positively related to BDNF
levels in the amygdala, but not in the hippocampus (Yee et al. 2007).
Figure 2. Models of LTP and LTD in the lateral nucleus (LA) of the amygdala (for a detailed escription,
see text)
