The article by Michael S. Fanselow and Joseph E. LeDoux discusses the role of the basolateral amygdala (ABL) in Pavlovian fear conditioning. They argue that the ABL is crucial for encoding the emotional component of fear memories and modulating the consolidation of these memories in other brain regions. Key evidence supporting this view includes: 1. **Lesion Studies**: Destruction of the ABL before training prevents learning, while lesions made after training prevent retention of fear memory. 2. **Neural Activity Changes**: Fear conditioning induces changes in neural activity in the ABL, such as enhanced responses to the conditional stimulus (CS) and long-term potentiation (LTP) in CS pathways. 3. **Disruption of Neural Activity**: Disrupting neural activity in the ABL during learning prevents learning, as shown by blocking NMDA receptors or increasing inhibition with drugs like AP5 and muscimol. The authors conclude that while the ABL is essential for implicit learning in fear conditioning, it may also be part of a distributed network that encodes fear memories. They suggest that the ABL's role is in encoding fear memories and modulating memory functions in other structures, rather than directly storing memories itself.The article by Michael S. Fanselow and Joseph E. LeDoux discusses the role of the basolateral amygdala (ABL) in Pavlovian fear conditioning. They argue that the ABL is crucial for encoding the emotional component of fear memories and modulating the consolidation of these memories in other brain regions. Key evidence supporting this view includes: 1. **Lesion Studies**: Destruction of the ABL before training prevents learning, while lesions made after training prevent retention of fear memory. 2. **Neural Activity Changes**: Fear conditioning induces changes in neural activity in the ABL, such as enhanced responses to the conditional stimulus (CS) and long-term potentiation (LTP) in CS pathways. 3. **Disruption of Neural Activity**: Disrupting neural activity in the ABL during learning prevents learning, as shown by blocking NMDA receptors or increasing inhibition with drugs like AP5 and muscimol. The authors conclude that while the ABL is essential for implicit learning in fear conditioning, it may also be part of a distributed network that encodes fear memories. They suggest that the ABL's role is in encoding fear memories and modulating memory functions in other structures, rather than directly storing memories itself.