MOLECULAR MECHANISMS OF FEAR LEARNING AND MEMORY

MOLECULAR MECHANISMS OF FEAR LEARNING AND MEMORY

2011 October 28; 147(3): 509–524 | Joshua P. Johansen, Christopher K. Cain, Linnaea E. Ostroff, and Joseph E. LeDoux
The article reviews the molecular mechanisms underlying fear learning and memory, focusing on Pavlovian fear conditioning. It highlights the role of synaptic plasticity in the lateral nucleus of the amygdala (LA) and discusses the neurotransmitter systems and signaling cascades involved in three phases of auditory fear conditioning: acquisition, consolidation, and reconsolidation. The review emphasizes the importance of Hebbian mechanisms, neuromodulatory regulation, and intracellular signaling pathways in these processes. Key findings include the involvement of NMDA receptors, CaMKII, protein kinases (PKA, PKC, MAPK), neurotrophin signaling, and presynaptic alterations in fear memory consolidation. The article also explores the role of PKMζ in memory maintenance and the concept of reconsolidation, where memories become labile upon reactivation, allowing for further modification. Overall, the research underscores the complexity of fear memory formation and the potential for understanding fear-related disorders through these molecular mechanisms.The article reviews the molecular mechanisms underlying fear learning and memory, focusing on Pavlovian fear conditioning. It highlights the role of synaptic plasticity in the lateral nucleus of the amygdala (LA) and discusses the neurotransmitter systems and signaling cascades involved in three phases of auditory fear conditioning: acquisition, consolidation, and reconsolidation. The review emphasizes the importance of Hebbian mechanisms, neuromodulatory regulation, and intracellular signaling pathways in these processes. Key findings include the involvement of NMDA receptors, CaMKII, protein kinases (PKA, PKC, MAPK), neurotrophin signaling, and presynaptic alterations in fear memory consolidation. The article also explores the role of PKMζ in memory maintenance and the concept of reconsolidation, where memories become labile upon reactivation, allowing for further modification. Overall, the research underscores the complexity of fear memory formation and the potential for understanding fear-related disorders through these molecular mechanisms.
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