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the dentate gyrus (Vouimba et al. 2007). Recent data obtained by stimulation of the BLA in
freely moving rats (Frey et al. 2001) support the view that hippocampal sensory information
can be stabilized by amygdaloidal influences. Activation of BLA inputs also facilitates LTP
induction at corticostriatal synapses (Popescu et al. 2007).
Beside the ability of LA and BLA neurons to develop long-term plasticity changes, which
will be discussed below, LTP can be also induced in the medial (Shindou et al. 1993;
Watanabe et al. 1995b) and the central nucleus of the amygdala (Ce) (Fu et al. 2007; Lopez
de and Sah 2007; Pollandt et al. 2006; Samson and Pare 2005). In addition, low- and high-
frequency stimulation of basolateral afferents, respectively, induce LTD and LTP of
responses in GABAergic intercalated cells of the amygdala (Royer and Pare 2002).
II.
LTP
IN THE
L
ATERAL
N
UCLEUS OF THE
A
MYGDALA AND
F
EAR
C
ONDITIONING
Pavlovian fear conditioning has emerged as a leading behavioral paradigm for studying
the neurobiological basis of learning and memory (Schafe et al. 2001).
Fear conditioning is a form of classical conditioning that depends on the amygdala
(LeDoux 2000; Maren 2001). The conditioned fear response is considered to be acquired by
rodents when a neutral conditioned stimulus (tone information) is combined with that of an
unconditioned stimulus (typically an electrical foot shock). The lateral nucleus of the
amygdala
(
LA
)
receives direct sensory inputs from the thalamus and cortex, and serves as the
sensory input station of the amygdala (Pitkanen et al. 1997). The LA sends direct and indirect
projections to the Ce, which in turn project to brainstem and to hypothalamic regions that
govern defensive behaviors and accompanying autonomic and endocrine responses (Pitkanen
et al. 1997). It is proposed that the LA activation as a sensory interface is limited to relatively
simple, unimodal conditioned stimulus features, whereas the BLA may serve as an
amygdaloid sensory interface for complex, configural conditioned stimulus information
(Yaniv et al. 2004).
The LA is a crucial site of neural changes that occur during fear conditioning. LTP within
the LA as an experience-dependent form of neural plasticity is believed to involve
mechanisms that underlie fear memory formation. A number of studies indicate that both fear
conditioning-induced neuronal plasticity and LTP at amygdaloid synapses share common
mechanisms of induction and expression (McKernan and Shinnick-Gallagher 1997; Rogan et
al. 1997). For example, McKernan and Shinnick-Gallagher (1997) have shown that fear-
potentiated startle training enhances the amplitude of synaptic currents in LA neurons in-
vitro. Fear conditioning also reduced paired pulse facilitation, in which the evoked response
to the second stimulus of a pair is larger than that to the first stimulus. This indicates that fear-
potentiated startle training had increased transmitter release in the thalamo-LA pathway. In
addition, Rogan et al. (1997) have demonstrated that auditory evoked potentials in the
thalamo-amygdaloid pathway are also augmented during the acquisition of auditory fear
conditioning. Furthermore, it was also observed that fear conditioning produces an LTP-like
enhancement of neurotransmitter release in the cortico-amygdaloid pathways, while reducing
LTP-induced enhancement of synaptic plasticity (Tsvetkov et al. 2002).
