Abstract
BackgroundPavlovian fear conditioning is a classical form of associative learning, which depends on associative synaptic plasticity in the amygdala. Recent findings suggest that the central amygdala (CeA) plays an active role in the acquisition of fear learning. However, little is known about the synaptic properties of the CeA in fear learning. The capsular part of the central amygdala (CeC) receives direct nociceptive information from the external part of the lateral parabrachial nucleus (lPB), as well as highly processed polymodal signals from the basolateral nucleus of the amygdala (BLA). Therefore, we focused on CeC as a convergence point for polymodal BLA signals and nociceptive lPB signals, and explored the synaptic regulation of these pathways in fear conditioning.ResultsIn this study, we show that fear conditioning results in synaptic potentiation in both lPB-CeC and BLA-CeC synapses. This potentiation is dependent on associative fear learning, rather than on nociceptive or sensory experience, or fear memory retrieval. The synaptic weight of the lPB-CeC and BLA-CeC pathways is correlated in fear-conditioned mice, suggesting that fear learning may induce activity-dependent heterosynaptic interactions between lPB-CeC and BLA-CeC pathways. This synaptic potentiation is associated with both postsynaptic and presynaptic changes in the lPB-CeC and BLA-CeC synapses.ConclusionsThese results indicate that the CeC may provide an important locus of Pavlovian association, integrating direct nociceptive signals with polymodal sensory signals. In addition to the well-established plasticity of the lateral amygdala, the multi-step nature of this association system contributes to the highly orchestrated tuning of fear learning.
Highlights
Pavlovian fear conditioning is a classical form of associative learning, which depends on associative synaptic plasticity in the amygdala
It is possible that information from the lateral parabrachial nucleus (lPB) and basolateral nucleus of the amygdala (BLA) pathways can be integrated by capsular part of the central amygdala (CeC) neurons in a cooperative manner during the fear learning process
We examined the behavior of these mice (Figure 1B) and analyzed the effects of the different procedures on evoked Excitatory postsynaptic current (EPSC) recorded at a holding potential of −60 mV in the presence of 100 μM picrotoxin at both lPB-CeC synapses and BLA-CeC synapses in vitro (Figure 1C, D and 2)
Summary
Pavlovian fear conditioning is a classical form of associative learning, which depends on associative synaptic plasticity in the amygdala. In Pavlovian fear conditioning, a previously emotionally neutral conditioned stimulus (CS) acquires the ability to elicit defensive responses when it is presented in conjunction with an aversive unconditioned stimulus (US) While this associative learning has been considered to occur within the lateral nucleus of the amygdala (LA), growing evidence suggests that the central nucleus of the amygdala (CeA), which was previously considered to function as a passive relay to. The CeC receives excitatory input from the basolateral nucleus of the amygdala (BLA), which transmits polymodal sensory information, including nociception, from thalamic and cortical regions [17,18,19,20,21] Together, these findings suggest that the CeC may be an important locus of CS-US association by integrating BLA and lPB signals
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