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Amygdala, Emotions and Memory

March 1, 2014

From Wikipedia

The amygdalae (singular: amygdala; from Greek for ‘almond’, ‘tonsil’) are almond-shaped groups of nuclei located deep and medially within the temporal lobes of the brain. Shown in research to perform a primary role in the processing of memory and emotional reactions, the amygdalae are considered part of the limbic system.

There are functional differences between the right and left amygdala. In one study, electrical stimulations of the right amygdala induced negative emotions, especially fear and sadness. In contrast, stimulation of the left amygdala was able to induce either pleasant (happiness) or unpleasant (fear, anxiety, sadness) emotions. Other evidence suggests that the left amygdala plays a role in the brain’s reward system.



The amygdala sends projections to the hypothalamus, the dorsomedial thalamus, the thalamic reticular nucleus, the nuclei of the trigeminal nerve and the facial nerve, the ventral tegmental area, the locus coeruleus, and the laterodorsal tegmental nucleus.[5]

Coronal section of brain through intermediate mass of third ventricle. Amygdala is shown in purple.

The cortical nucleus is involved in the sense of smell and pheromone-processing. It receives input from the olfactory bulb and olfactory cortex. The lateral amygdalae, which send impulses to the rest of the basolateral complexes and to the centromedial nuclei, receive input from the sensory systems. The centromedial nuclei are the main outputs for the basolateral complexes, and are involved in emotional arousal.

Emotional learning

In complex vertebrates, including humans, the amygdalae perform primary roles in the formation and storage of memories associated with emotional events. Research indicates that, during fear conditioning, sensory stimuli reach the basolateral complexes of the amygdalae, particularly the lateral nuclei, where they form associations with memories of the stimuli. The association between stimuli and the aversive events they predict may be mediated by long-term potentiation, a sustained enhancement of signaling between affected neurons.[3]

Memories of emotional experiences imprinted in reactions of synapses in the lateral nuclei elicit fear behavior through connections with the central nucleus of the amygdalae and the bed nuclei of the stria terminalis (BNST). The central nuclei are involved in the genesis of many fear responses such as defensive behavior (freezing or escape responses), autonomic nervous system responses (changes in blood pressure and heart rate/tachycardia), neuroendocrine responses (stress-hormone release), etc. Damage to the amygdalae impairs both the acquisition and expression of Pavlovian fear conditioning, a form of classical conditioning of emotional responses.[3]

The amygdalae are also involved in appetitive (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 nuclei.[17] However, lesions of the central nucleus in the amygdala have been shown to reduce appetitive learning in rats. Lesions of the basolateral regions do not exhibit the same effect.[18] Research like this indicates that different nuclei within the amygdala have different functions in appetitive conditioning.[19]

Memory modulation

The amygdala is also involved in the modulation of memory consolidation. Following any learning event, the long-term memory for the event is not formed instantaneously. Rather, information regarding the event is slowly assimilated into long-term (potentially lifelong) storage over time, possibly via long-term potentiation. Recent studies suggest that, while the amygdala is not itself a long-term memory storage site, and learning can occur without it, one of its roles is to regulate memory consolidation in other brain regions.[20] Also, fear conditioning, a type of memory that is impaired following amygdala damage, is mediated in part by long-term potentiation.[21][22]

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. The amygdala are involved in mediating the effects of emotional arousal on the strength of the memory for the event.

Buddhist monks who do compassion meditation have been shown to modulate their amygdala, along with their temporoparietal junction and insula, during their practice.[25] In an fMRI study, more intensive insula activity was found in expert meditators than in novices.[26] Increased activity in the amygdala following compassion-oriented meditation may contribute to social connectedness.[27]

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 amygdalar activity, and that activity correlates with retention. Amygdala neurons show various types of oscillation during emotional arousal, such as theta activity. These synchronized neuronal events could promote synaptic plasticity (which is involved in memory retention) by increasing interactions between neocortical storage sites and temporal lobe structures involved in declarative memory.[28]

Research using Rorschach test blot 03 finds that the number of unique responses to this random figure links to larger sized amygdalae. The researchers note, “Since previous reports have indicated that unique responses were observed at higher frequency in the artistic population than in the nonartistic normal population, this positive correlation suggests that amygdalar enlargement in the normal population might be related to creative mental activity.”[29]

Neuropsychological correlates of amygdala activity

As early as 1888, rhesus monkeys with a lesioned temporal cortex (including the amygdala) were observed to have significant social and emotional deficits.[30] Heinrich Klüver and Paul Bucy later expanded upon this same observation by showing that large lesions to the anterior temporal lobe produced noticeable changes, including overreaction to all objects, hypoemotionality, loss of fear, hypersexuality, and hyperorality, a condition in which inappropriate objects are placed in the mouth. Some monkeys also displayed an inability to recognize familiar objects and would approach animate and inanimate objects indiscriminately, exhibiting a loss of fear towards the experimenters. This behavioral disorder was later named Klüver-Bucy syndrome accordingly,[31] and later research proved it was specifically due to amygdala lesions. Monkey mothers who had amygdala damage showed a reduction in maternal behaviors towards their infants, often physically abusing or neglecting them.[32] In 1981, researchers found that selective radio frequency lesions of the whole amygdala caused Klüver-Bucy Syndrome.[33]

With advances in neuroimaging technology such as MRI, neuroscientists have made significant findings concerning the amygdala in the human brain. A variety of data shows the amygdala has a substantial role in mental states, and is related to many psychological disorders. Some studies have shown children with anxiety disorders tend to have a smaller left amygdala. In the majority of the cases, there was an association between an increase in the size of the left amygdala with the use of SSRI‘s (antidepressant medication) or psychotherapy. The left amygdala has been linked to social anxiety, obsessive and compulsive disorders, and post traumatic stress, as well as more broadly to separation and general anxiety.[34] In a 2003 study, subjects with borderline personality disorder showed significantly greater left amygdala activity than normal control subjects. Some borderline patients even had difficulties classifying neutral faces or saw them as threatening.[35] Individuals with psychopathy show reduced autonomic responses, relative to comparison individuals, to instructed fear cues.[36] In 2006, researchers observed hyperactivity in the amygdala when patients were shown threatening faces or confronted with frightening situations. Patients with more severe social phobia showed a correlation with increased response in the amygdala.[37] Similarly, depressed patients showed exaggerated left amygdala activity when interpreting emotions for all faces, and especially for fearful faces. Interestingly, this hyperactivity was normalized when patients were administered antidepressant medication.[38] By contrast, the amygdala has been observed to respond differently in people with bipolar disorder. A 2003 study found that adult and adolescent bipolar patients tended to have considerably smaller amygdala volumes and somewhat smaller hippocampal volumes.[39] Many studies have focused on the connections between the amygdala and autism.[40]

Studies in 2004 and 2006 showed that normal subjects exposed to images of frightened faces or faces of people from another race will show increased activity of the amygdala, even if that exposure is subliminal.[41][42] However, the amygdala is not necessary for the processing of fear-related stimuli, since persons in whom it is bilaterally damaged show rapid reactions to fearful faces, even in the absence of a functional amygdala.

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