Abstract

The central, lateral and basolateral amygdala (BLA) nuclei are essential for the formation of long-term memories including emotional and drug-related memories. Studying cellular and molecular mechanisms of memory in amygdala may lead to better understanding of how memory is formed and of fear and addiction-related disorders. A challenge is to identify molecules activated by learning that subserve cellular changes needed for memory formation and maintenance in amygdala. Recent studies show that activation of synaptic receptors during fear and drug-related learning leads to alteration in actin cytoskeleton dynamics and structure in amygdala. Such changes in actin cytoskeleton in amygdala are essential for fear and drug-related memories formation. Moreover, the actin cytoskeleton subserves, after learning, changes in neuronal morphogenesis and glutamate receptors trafficking in amygdala. These cellular events are involved in fear and drug-related memories formation. Actin polymerization is also needed for the maintenance of drug-associated memories in amygdala. Thus, the actin cytoskeleton is a key mediator between receptor activation during learning and cellular changes subserving long-term memory (LTM) in amygdala. The actin cytoskeleton may serve as a target for pharmacological treatment of fear memory associated with fear and anxiety disorders and drug addiction to prevent the debilitating consequences of these diseases.

Highlights

  • This review describes and discusses the mechanisms whereby actin cytoskeleton in amygdala mediates fear and drug-associated memory formation

  • The above studies lead to several additional insights: (1) actin is needed for basic neuronal functions including synaptic transmission and morphogenesis interfering with functions of actin cytoskeleton in amygdala has no effect on fear memory acquisition but on its consolidation

  • A tenable hypothesis is that actin cytoskeleton affects neuronal functions in amygdala needed for fear memory consolidation; (2) The actin cytoskeleton in amygdala is involved in maintenance of certain memories

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Summary

Raphael Lamprecht*

Reviewed by: Tija Jacob, University of Pittsburgh School of Medicine, USA Roger Lee Clem, Icahn School of Medicine at Mount Sinai, USA. Studying cellular and molecular mechanisms of memory in amygdala may lead to better understanding of how memory is formed and of fear and addiction-related disorders. A challenge is to identify molecules activated by learning that subserve cellular changes needed for memory formation and maintenance in amygdala. Recent studies show that activation of synaptic receptors during fear and drug-related learning leads to alteration in actin cytoskeleton dynamics and structure in amygdala. Such changes in actin cytoskeleton in amygdala are essential for fear and drug-related memories formation. The actin cytoskeleton subserves, after learning, changes in neuronal morphogenesis and glutamate receptors trafficking in amygdala These cellular events are involved in fear and drug-related memories formation.

INTRODUCTION
MODULATION OF ACTIN CYTOSKELETON IN AMYGDALA BY LEARNING
Actin in Neuronal Morphogenesis
Actin in Glutamate Receptors Trafficking
ARE CHANGES IN ACTIN POLYMERIZATION NEEDED FOR THE MAINTENANCE OF MEMORY?
CONCLUSIONS AND DISCUSSION
ACTIN CYTOSKELETON IN AMYGDALA MEDIATES BETWEEN LEARNING AND MEMORY FORMATION
FUTURE RESEARCH
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