ReDes De Amigdala

Abstract
The last ten years have witnessed a surge of interest for the mechanisms underlying the acquisition and extinction of classically conditioned fear responses. In part, this results from the realization that abnormalities in fear learning mechanisms likely participate to the development and/or maintenance of human anxiety disorders. The simplicity and robustness of this learning paradigm,coupled to the fact that the underlying circuitry is evolutionarily well conserved makes it an ideal model to study the basic biology of memory and identify genetic factors and neuronal systems that regulate the normal and pathological expressions of learned fear. Critical advances have been made in determining how modified neuronal functions upon fear acquisition become stabilized during fearmemory consolidation and how these processes are controlled in the course of fear memory extinction. With these advances, came the realization that activity in remote neuronal networks must be coordinated for these events to take place. In this paper, we review these mechanisms of coordinated network activity and the molecular cascades leading to enduring fear memory, and allowing for theirextinction. We will focus on Pavlovian fear conditioning as a model and the amygdala as a key component for the acquisition and extinction of fear responses.
Keywords: Pavlovian fear conditioning, extinction, prefrontal cortex, hippocampus, synaptic plasticity, oscillations
*  Other Sections▼
* Abstract
* I. Introduction: The Case for an Animal Model of Fear and Anxiety
* II.Structure and connectivity of the amygdala
* III. Oscillatory Activity During Fear Learning and Emotional Arousal
* IV. Synaptic plasticity in the amygdala related to conditioned fear
* V. Synaptic Plasticity Related to Fear Extinction
* VI. Conclusions: Relation Between Fear and Extinction Memories
* References
I. Introduction: The Case for an Animal Model ofFear and Anxiety
Fear and anxiety are adaptive responses generated in anticipation or in the presence of stimuli that threaten to perturb homeostasis. While fear is generally elicited by particular cues or contexts, anxiety can occur in the absence of these triggers (88). Fear and anxiety are exhibited by all mammals, including humans, and appear to be part of a universal survival strategy. Notsurprisingly, these states are controlled by a hierarchy of neural systems, which determine the efficacy of the responses and permit dynamic adaptations, thereby ensuring appropriate emotional responses and return to baseline activity once the threat has passed. Extreme variations or perturbations of these mechanisms can lead to prolonged (even irreversible) and disproportional states with respect tothe triggering stimulus, persistence of anxiety following withdrawal of the stimulus, or omnipresent generalized anxiety. In their extreme or pathological forms, these states include panic disorders, phobias, and posttraumatic stress disorders (510, 523). These are common diseases with an estimated lifetime prevalence of up to 18% (8, 200), imposing a major challenge to health providers and burdenon the economy. A large body of evidence indicates that these states are under genetic and environmental control, during early development as well as later in life, determining inter-individual variations (for review see (143)). Genome-wide linkage analysis and association studies have indeed led to identification of a number of genetic factors that determine the heritability of anxietydisorders, although the wide spectrum of symptoms and restricted sample sizes have limited success so far (143, 163).
The motivation for developing animal models of fear and anxiety is thus twofold. First, animal models allow the study of single-gene modifications in a well-defined genetic background and under controlled environmental conditions, thereby partly overcoming problems inherent to human...