Amygdala

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Image:Amyg.png The amygdala (Latin, corpus amygdaloideum) is an almond-shaped set of neurons located deep in the brain's medial temporal lobe. Shown to play a key role in the processsing of emotions, the amygdala forms part of the limbic system. In humans and other animals, this subcortical brain structure is linked to both fear responses and pleasure. Its size is positively correlated with aggressive behavior across species. In humans, it is the most sexually-dimorphic brain structure, and shrinks by more than 30% in males upon castration. Conditions such as anxiety, autism, depression, post-traumatic stress disorder, and phobias are suspected of being linked to abnormal functioning of the amygdala, owing to damage, developmental problems, or neurotransmitter imbalance.

1 Anatomical subdivisions
- 1.1 Connections
2 Emotional learning and memory
3 Memory modulation and drug addiction
4 See also
5 References
6 External links:

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Anatomical subdivisions

The amygdala is actually several separately-functioning nuclei that anatomists group together by the proximity of the nuclei to one another. Key among these nuclei are the basolateral complex, the centromedial nucleus, and the cortical nucleus.

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Connections

The basolateral complex receives input from the sensory systems, and is necessary for fear conditioning in rats. The centromedial nucleus is the main output for the basolateral complex, and is involved in emotional arousal in rats and cats. The amygdala sends outputs to the hypothalamus for activation of the sympathetic nervous system, the reticular nucleus for increased reflexes, the nuclei of the trigeminal nerve and facial nerve for facial expressions of fear, and the ventral tegmental area, locus ceruleus, and laterodorsal tegmental nucleus for activation of dopamine, norepinephrine and epinephrine. The cortical nucleus is involved in olfaction and pheromone-processing. It receives input from the olfactory bulb and olfactory cortex.

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Emotional learning and memory

A key function of the amygdala in complex vertebrates, including humans is forming and storing memories for emotional events. Damage to the amygdala impairs both the acquisition and expression of Pavlovian fear conditioning, a form of classical conditioning of emotional responses. Considerable research indicates that, during fear conditioning, sensory stimuli reach the basolateral complex, particularly the lateral nucleus of the amygdala, where they become associated. The association between stimuli and the aversive events they predict may be mediated by long-term potentiation, a form of long-lasting synaptic plasticity. Memories of emotional experiences stored in lateral nucleus synapses elicit fear behavior though connections with the central nucleus of the amygdala, a center involved in the genesis of many fear responses, including freezing (immobility), tachycardia (rapid heartbeat), increased respiration, and stress-hormone release.

The amygdala also plays a role in apetitive (positive) conditioning. It seems that distinct neurons respond to positive and negative stimuli, but there is no clustering of these distinct neurons into clear anatomical nucleiTemplate:Ref.

The suppression of learned fear responses is an important goal of therapeutic interventions for disorders of fear and anxiety, such as post-traumatic stress disorder and phobias, in humans. Evidence suggests that the amygdala is involved not only in fear conditioning, but also in the extinction of fear responses. Extinction, which occurs when fear signals are presented alone several times, yields a reduction in fear responses to those signals. Extinction training does not eliminate the fear memory, however; it is accompanied by new learning that inhibits the original fear. It is interesting to note that extinction learning (at least for fear responses) may also require synaptic plasticity in the amygdala. Systematic desensitization is a type of behavioral therapy for anxiety that relies on extinction learning.

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Memory modulation and drug addiction

The amygdala also plays a key role in the modulation of memory consolidation. Following any learning event, the long-term memory for the event is not instantaneously formed. Rather, information regarding the event is slowly put into long-term storage over time, a process referred to as memory consolidation, until it reaches a relatively permanent state. During the consolidation period, the memory can be modulated. In particular, it appears that emotional arousal following the learning event influences the strength of the subsequent memory for that event. Greater emotional arousal following a learning event enhances a person's retention of that event. Experiments have shown that administration of stress hormones to individuals immediately after they learn something enhances their retention when they are tested two weeks later.

The amygdala, especially the basolateral amygdala, plays a key role in mediating the effects of emotional arousal on the strength of the memory for the event, as shown by many laboratories including that of James McGaugh. These laboratories have trained animals on a variety of learning tasks and found that drugs injected into the amygdala after training affect the animals' subsequent retention of the task. These tasks include basic Pavlovian tasks such as inhibitory avoidance (where a rat learns to associate a mild footshock with a particular compartment of an apparatus) and more complex tasks such as spatial or cued water maze (where a rat learns to swim to a platform to escape the water). If a drug that activates the amygdala is injected into the amygdala, the animal has better memory for the training in the task. If a drug that inactivates the amygdala is injected into it, the animal has impaired memory for the task.

Despite the importance of the amygdala in modulating memory consolidation, however, learning can occur without it, though such learning appears to be impaired, as in fear conditioning impairments following amygdala damage.

Evidence from work with humans indicates that the amygdala plays a similar role. Amygdala activity at the time of encoding information correlates with retention for that information. However, this correlation depends on the relative "emotionalness" of the information. More emotionally-arousing information increases amygdala activity, and that activity correlates with retention.

Experiments with rats also suggest that the amygdala is involved in learning about various cues with the consumption of drugs of abuse. It is well-known that one of the major problems in drug addiction is that drug-associated cues induce significant craving in individuals, even if the individuals have not taken the drugs in a long time. The amygdala appears to play a key role in the initial learning of the association between the cues and the drugs. In addition, inactivation of the amygdala prevents the ability of cues to induce reinstatement in rats in a drug self-administration paradigm.

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