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Fear memories require protein synthesis in the amygdala for reconsolidation after retrieval
TLDR
It is shown that consolidated fear memories, when reactivated during retrieval, return to a labile state in which infusion of anisomycin shortly after memory reactivation produces amnesia on later tests, regardless of whether reactivation was performed 1 or 14 days after conditioning.
NMDA Receptors and L-Type Voltage-Gated Calcium Channels Contribute to Long-Term Potentiation and Different Components of Fear Memory Formation in the Lateral Amygdala
TLDR
The results suggest that two pharmacologically distinct forms of LTP can be isolated in the LA in vitro and that a combination of both contribute to the formation of fear memories in vivo at the cellular level.
Activation of ERK/MAP Kinase in the Amygdala Is Required for Memory Consolidation of Pavlovian Fear Conditioning
TLDR
It is shown that ERK/MAPK activation is necessary for both memory consolidation of Pavlovian fear conditioning and synaptic plasticity in the amygdala and bath application of U0126 impairs long-term potentiation in the LA in vitro.
Reply — reconsolidation: The labile nature of consolidation theory
TLDR
It is argued that consolidation is not a one-time event, but instead is reiterated with subsequent activation of the memories, opening up a new dimension in the study of memory consolidation.
Rethinking the Fear Circuit: The Central Nucleus of the Amygdala Is Required for the Acquisition, Consolidation, and Expression of Pavlovian Fear Conditioning
TLDR
Using functional inactivation methods, it is shown that CE is involved not only in the expression of fear expression but also the acquisition of fear conditioning and that inhibition of protein synthesis in CE after training impairs fear memory consolidation.
Memory Consolidation of Auditory Pavlovian Fear Conditioning Requires Protein Synthesis and Protein Kinase A in the Amygdala
TLDR
It is suggested that the LA is essential for memory consolidation of auditory fear conditioning and that this process is PKA and protein-synthesis dependent.
Estradiol-Induced Enhancement of Object Memory Consolidation Involves Hippocampal Extracellular Signal-Regulated Kinase Activation and Membrane-Bound Estrogen Receptors
TLDR
This study is the first to identify a specific molecular pathway by which E2 modulates memory and to demonstrate a novel role for membrane-bound ERs in mediating E2-induced improvements in hippocampal memory consolidation.
Synaptic plasticity in the lateral amygdala: a cellular hypothesis of fear conditioning.
TLDR
It is proposed that the CS evokes EPSPs at sensory input synapses onto LA pyramidal neurons, and that the US strongly depolarizes these same LA neurons, which induce LTP-like changes that store memories during fear conditioning.
The Group I Metabotropic Glutamate Receptor mGluR5 Is Required for Fear Memory Formation and Long-Term Potentiation in the Lateral Amygdala
TLDR
The results of this study indicate that mGluR5 in the LA plays a crucial role inFear conditioning and in plasticity at synapses involved in fear conditioning.
Memory consolidation for contextual and auditory fear conditioning is dependent on protein synthesis, PKA, and MAP kinase.
TLDR
Experiments examined whether inhibition of protein synthesis, PKA, and MAP kinase activity, treatments that block LTP, also interfere with the consolidation of fear conditioning, and indicated that injection of these compounds selectively interfered with long- term memory for contextual and auditory fear, while leaving short-term memory intact.
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