Biology Reference
In-Depth Information
accordance with data from Lin et al. (2000), but in contrast to data from Wang and Gean
(1999), we found that LA-LTD induced by intranuclear stimulation was accompanied by an
enhancement in the paired pulse ratio, indicating that LA-LTD results from an decrease in
transmitter release probability (unpublished observation). This implicates
an involvement of a
presynaptic expression mechanism of LA-LTD. These results and other findings described for
BLA neurons support the hypothesis that two forms of LTD coexist at the same LA synapses.
Both, induction and expression mechanisms appear to be different; one is dependent on group
II mGluRs and seems to be predominantly expressed presynaptically, whereas the other is
NMDA receptor-dependent and seems to be expressed postsynaptically.
D. Depotentiation of LA-LTP and reversal of LA-LTD
The question arose whether LTP or LTD in the LA passes through a consolidation period
during which it is susceptible to disruption. When delivered to the intranuclear pathway 10
min after LTP induction, a 15 min episode of LFS (1 Hz) permanently erased LTP. However,
when administered at a delay of 20 min, the same treatment did not have a strong impact on
established LTP. These results provide the first evidence of the limited vulnerability of LA-
LTP to be reversed by LFS and may support the assumption that LTP stabilization
mechanisms in the LA take less than 20 min at least when intranuclear fibers were stimulated.
When EC fibers were stimulated to induce LTP in the BLA, a LFS-induced depotentiation
was even possible 35 min after HFS (Aroniadou-Anderjaska et al. 2001). Therefore, we
repeated the depotentiation experiments using EC-stimulation. In contrast to intranuclear
stimulation, LFS was not able to erase LTP, when delivered to the EC pathway 10 min after
LTP induction. However, LFS given 20 min after LTP induction permanently erased LTP
(Drephal et al. 2006). Therefore, LTP in the LA exhibits vulnerability at different time
windows in dependence of the kind of used afferents. In contrast to the BLA (Aroniadou-
Anderjaska et al. 2001) LFS did not cause a complete depotentiation when applied 35 min
after LTP induction in the LA.
In some instances, low-frequency stimuli that are normally subthreshold for inducing
homosynaptic LTD can induce LTD, if the pathway has been previously potentiated. This
effect has been reported for LFS in coronal slices from the BLA (Aroniadou-Anderjaska et al.
2000; Li et al. 1998). It can be supposed that the induction of LTP, like priming stimulation,
lowers the threshold for the subsequent induction of homosynaptic LTD. Our data indicate
that the reversal of LTD can be induced by TBS as well as by HFS when the stimulus was
delivered ≤ 20 min after LFS at these synapses. The delivery of weak TBS enhanced
depressed fEPSPs to approximately pre-LFS control levels. The delivery of HFS resulted not
only in a reversal, but it potentiated fEPSPs at a higher degree than HFS-induced LTP
delivered in naive (“non-primed”) slices (Kaschel et al. 2004). Our results also support
previous data that induction of synaptic plasticity can be influenced by prior neuronal activity
It is known that several neurotransmitter systems are implicated in the mediation of
depotentiation. When LFS is delivered 10 min after HFS to the EC-LA pathway,
depotentiation is dependent on the serine/threonine protein phosphatase calcineurin (Lin et al.
2003b) along with the involvement of NMDARs. It is to note that GABA antagonists were
used in the study of Lin et al. (2003b). However, since we did not find a depotentiation of
LTP when LFS was delivered 10 min after HFS, it can be suggested that susceptibility to
