Biology Reference
In-Depth Information
disruption of LA-LTP by LFS could also be due to different kinds of afferents running
through the EC in coronal and horizontal slices.
E. LTP in interneurons of the LA
The lateral amygdala contains several subpopulations of inhibitory interneurons that
represent nearly 25% of the neurons in the LA (McDonald and Augustine 1993) and can be
distinguished on the basis of their content of calcium-binding proteins or peptides.
Interneurons can also identified morphologically by their aspiny dendritic trees and
physiologically by their ability to generate high frequency, non-adapting spike trains in
response to depolarizing current pulses (Lang and Pare 1998; Rainnie et al. 1991; Sah et al.
2003).
It is well known that the ability to induce LTP in LA projection neurons in vitro
depends on the strength of the local inhibitory network. At least in the BLA, GABAergic
local circuit neurons might possess AMPA receptors with higher calcium permeability on
average than pyramidal cells, as it has been suggested for hippocampus (He et al. 1999). An
involvement of GABAergic interneurons in NMDA-dependent LTP in the amygdala is
controversially discussed. Whereas Mahanty and Sah (1998) reported that LTP in GABAergic
interneurons in the BLA is AMPAR-dependent, Bauer and LeDoux (2004) demonstrated an
involvement of NMDA receptors in LA-LTP of GABAergic interneurons.
F. Retrograde signaling
As described above LA-LTP and LA-LTD are triggered postsynaptically and, at least in
part, their expressions depend on presynaptic mechanisms. From the hippocampus it is known
that different retrograde messengers exist that can be released from the postsynaptic dendrite
and diffuse back across the synapse to increase neurotransmitter release. Several candidates
including lipid mediators such as arachidonic acid or one of its lipoxygenase metabolites,
platelet-activating factor, and neuroactive gaseous substances, such as nitric oxide (NO) and
carbon monoxide, have attracted much interest (Medina and Izquierdo 1995). Real progress
has been made in clarifying the possible role of nitric oxide as a retrograde messenger. We
and others have shown that TBS-induced CA1-LTP is NO-dependent, since CA1-LTP is
blocked by the unspecific NO-synthetase inhibitor N
G
-nitro-L-arginine-methyl-ester (L-
NAME). We used the dye 1,2-diaminoanthraquinone (DAQ) to demonstrate NO production
in rat brain slices in relation to induction of LTP. We found that DAQ induced fluorescence is
elevated within a limited area of about 40000 µm
2
during LTP-induction in the hippocampal
area CA1 (von Bohlen und Halbach et al. 2002). L-NAME was able to inhibit the induction of
LTP, accompanied by a strong reduction of DAQ induced fluorescence.
Although the neuronal nitric oxide synthetase (n-NOS) is localized in the LA (Schafe et
al. 2005), EC-induced LA-LTP recorded in coronal slices was unaffected by inhibition of
endogenous NO (Watanabe et al. 1995b). We recently studied LA-LTP which was induced in
horizontal brain slices of wild types mice (C57BL/6J), mice homozygous for disruption of the
endothelial nitric oxide synthetase gene (eNOS
-/-
) and the nNOS gene (nNOS
-/-
). HFS of EC
fibers caused a reduced LA-LTP in both e-NOS
-/-
and the n-NOS
-/-
mice (unpublished
observation). Along this line, a decrease in the magnitude of hippocampal LTP has been
