Paré Denis, Quirk Gregory J, Ledoux Joseph E
Center for Molecular and Behavioral Neuroscience, Rutgers State University, 197 University Ave., Newark, NJ 07102, USA.
J Neurophysiol. 2004 Jul;92(1):1-9. doi: 10.1152/jn.00153.2004.
It is currently believed that the acquisition of classically conditioned fear involves potentiation of conditioned thalamic inputs in the lateral amygdala (LA). In turn, LA cells would excite more neurons in the central nucleus (CE) that, via their projections to the brain stem and hypothalamus, evoke fear responses. However, LA neurons do not directly contact brain stem-projecting CE neurons. This is problematic because CE projections to the periaqueductal gray and pontine reticular formation are believed to generate conditioned freezing and fear-potentiated startle, respectively. Moreover, like LA, CE may receive direct thalamic inputs communicating information about the conditioned and unconditioned stimuli. Finally, recent evidence suggests that the CE itself may be a critical site of plasticity. This review attempts to reconcile the current model with these observations. We suggest that potentiated LA outputs disinhibit CE projection neurons via GABAergic intercalated neurons, thereby permitting associative plasticity in CE. Thus plasticity in both LA and CE would be necessary for acquisition of conditioned fear. This revised model also accounts for inhibition of conditioned fear after extinction.
目前认为，经典条件性恐惧的习得涉及外侧杏仁核（LA）中条件性丘脑输入的增强。相应地，LA细胞会兴奋中央核（CE）中更多的神经元，这些神经元通过其向脑干和下丘脑的投射引发恐惧反应。然而，LA神经元并不直接接触投射到脑干的CE神经元。这是个问题，因为CE向导水管周围灰质和脑桥网状结构的投射分别被认为会产生条件性僵住和恐惧增强的惊吓反应。此外，与LA一样，CE可能会接收直接的丘脑输入，传递有关条件性和非条件性刺激的信息。最后，最近的证据表明，CE本身可能是可塑性的关键位点。本综述试图使当前模型与这些观察结果相协调。我们认为，增强的LA输出通过GABA能中间神经元解除对CE投射神经元的抑制，从而使CE中产生联合可塑性。因此，LA和CE中的可塑性对于条件性恐惧的习得都是必要的。这个修订后的模型也解释了消退后对条件性恐惧的抑制。
