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depending on their subunit composition (NR1, NR2A, NR2B, and NR2C and NR2D) (Cull-
Candy et al. 2001; Dingledine et al. 1999). These subunits are structurally related, with less
than 20% sequence identity, to other excitatory amino acid receptor subunits (Monyer et al.
1992). Pyramidal cells of the LA receive convergent inputs from the cortex, thalamus and
basal nuclei. At all inputs, AMPA, kainate and NMDA receptors are active and co-localized
in the postsynaptic density (Mahanty and Sah 1999). In both, cortical (Farb and LeDoux
1999) and thalamic (Farb and LeDoux 1997) afferent synapses anatomical evidence for
NMDARs has been found. The role of NMDARs is discussed controversially in basal
synaptic transmission and in LTP in the amygdala (for review, see Chapman and Chattarji
2000). The disparities may be explained by differences in inputs stimulated and experimental
paradigms. Since in very young animals excitatory postsynaptic potentials (EPSPs) or field
potentials included some NMDA receptor mediated activity (Aroniadou-Anderjaska et al.
2001; Mahanty and Sah 1999; Weisskopf and LeDoux 1999), an age-dependent shift can be
suggested. In adult rats we did not observe an involvement of NMDA receptors in basal
transmission (Drephal et al. 2006). The lack of effects of the NMDA receptor antagonist APV
on normal synaptic transmission in the LA of adult rodents was also observed in coronal
slices during EC stimulation
(Huang and Kandel 1998; Schroeder and Shinnick-Gallagher
2004).
Although it was suggested that HFS-induced LTP is not NMDA dependent (Chapman
and Bellavance 1992a; Watanabe et al. 1995a), our results suggest that both TBS- and
HFS-
induced LA-LTP are dependent on NMDARs (Drephal et al. 2006). APV reduced HFS-
induced LTP in all our studies in accordance with studies in coronal slices (Huang and
Kandel 1998; Schroeder and Shinnick-Gallagher 2004; Tsvetkov et al. 2002). Since we
obtained similar results for both, intracellular and extracellular recordings, it can be suggested
that field potentials in the LA authentically
reflect synaptic events.
In coronal slices, postsynaptically induced forms of homosynaptic LA-LTP were
described at cortical (Huang and Kandel 1998) as well as thalamic inputs (Bauer et al. 2002).
At thalamic input synapses LTP can be induced by using a pairing protocol in which weak
presynaptic stimulation of thalamo-amygdala afferents is presented concurrently with brief
depolarization of the postsynaptic cell by current injection (Bauer et al. 2001; Bauer et al.
2002; Schafe et al. 2000; Weisskopf et al. 1999).
Two pharmacologically distinct forms of LTP can be distinguished at thalamic input
synapses to the LA: LTP dependent on L-type VGCCs or on NMDARs. It has been suggested
that back-propagating action potentials invade the dendrites during pairing and interact with
EPSPs, leading to calcium entry through VGCCs. When trains of 10 stimuli at 30 Hz were
paired with 1 nA, 5 ms depolarizations given 5-10 ms after the onset of each EPSP in the
train, then this pattern yields an action potential at the peak of each EPSP of the train (Bauer
et al. 2002). NMDA dependent LTP can be induced by a 30 Hz tetanus (100 stimuli, given
twice with a 20s interval) (Bauer et al. 2002). This protocol did not trigger action potentials
but rather produced a long depolarization of the postsynaptic cell. Recently, it has been shown
that large dendritic spines contacted by thalamic afferents exhibited larger Ca
2+
transients
during action potential backpropagation than did small dendritic spines contacted by cortical
afferents (Humeau et al. 2005).
It is known that NMDA receptor blockade leads to a deficit in long- and short-term
memory of fear conditioning (Walker and Davis 2000). Whereas intra-amygdala blockade of
the NR2B subunit of the NMDA receptor disrupts the acquisition but not the expression of
