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intranuclear afferents were stimulated (Albrecht et al. 2003; Drephal et al. 2006; Pollandt et
al. 2003). In older rats (> 16 weeks) we could not induce TBS-induced LA-LTP. In addition,
whereas both TBS and HFS of afferents running through the LA induced stable LA-LTP,
TBS failed to induce LTP of EC-inputs to the LA. However, the low probability to induce
TBS-induced in an non-laminated structure as the LA confirm data obtained in coronal slices,
where TBS-induced LTP was dependent on additional stimulation of serotonin HT2 receptors
(Chen et al. 2003).
Many studies have shown that LTP can be induced in the amygdala (Chapman and
Chattarji 2000), however, only few studies indicate that
LTD did occur in neurons of the LA.
LTD, as a use-dependent decrease in synaptic strength, may increase the flexibility of
neuronal circuits within the amygdala. The first study which has documented LA-LTD in
coronal slices (Heinbockel and Pape 2000) used theta pulse stimulation (TPS; 8 Hz for 150
sec) of thalamic input fibers. This stimulation resulted in LA-LTD in 21% of the tested
neurons. The same stimulation delivered to cortical afferents (stimulation of EC fibers) did
not provoke long-term depression of LA activity. We found that TPS of afferents within the
LA caused a weaker LTD in horizontal slices than low frequency stimulation (900 pulses, 1
Hz - LFS) (Schubert et al. 2005). Although we have shown that the stimulation of EC fibers
did not produce significant LTD in rats (Kaschel et al. 2004), we tested LFS of EC fibers in
mice. In accordance with our previous results (Kaschel et al. 2004) as well as with results
obtained in coronal slices (Heinbockel and Pape 2000) we did not observe LTD of field
potential amplitudes when single pulse EC stimulation was used. However, using low
frequency paired pulse stimulation of EC fibers with an interstimulus interval of 40 ms, LA-
LTD can be provoked at least in the majority of recordings (unpublished observations). These
data suggest that excitatory afferents from the entorhinal cortex also activate GABAergic
interneurons within the LA. Paired pulse stimulation seems to cause a higher increase in
intracellular calcium and thereby facilitates the induction of LA-LTD. LTD within the LA
could enhance the relative effect of LTP at neighbouring
synapses, by increasing the signal-
to-noise ratio as shown recently for the amygdala (Royer and Pare 2003).
B. NMDARs, voltage-gated calcium channels (VGCCs) and mGluRs
Glutamatergic transmission is mediated by ionotropic and
metabotropic glutamate
receptors.
Ionotropic glutamate receptors are subdivided into three groups: α-amino-3-
hydroxy-5-methyl-4-isoxazole propionic acid (AMPA), N-methyl-D-aspartate (NMDA) and
kainate receptors. Metabotropic glutamate receptors
(mGluRs)
are divided into eight known
subtypes and three groups based on sequence homology, second messenger coupling and
pharmacology (Dingledine et al. 1999). In previous experiments we could show that field
potentials in horizontal slices of the LA were largely blocked by the AMPA and kainate
receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) (Pollandt et al. 2003).
Similar results were obtained in coronal slices (Lin et al. 2001). These results support the
conclusion that glutamate is the main transmitter at excitatory LA-synapses (Huang et al.
2000; Weisskopf et al. 1999).
It is known that the NMDA receptor (NMDAR)
subtype of glutamate-gated ion channels
is co-agonized by glycine and possesses high calcium permeability as well as a voltage-
dependent block by extracellular magnesium. NMDA receptors show unique properties
