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 lingering potential for affected synapses to react more readily.
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 stria terminalis (BNST). The central nuclei are involved in the genesis of many fear responses, including freezing (immobility), tachycardia (rapid heartbeat), increased respiration, and stress-hormone release. Damage to the amygdalae impairs both the acquisition and expression of Pavlovian fear conditioning, a form of classical conditioning of emotional responses. 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. Different nuclei within the amygdala have different functions in appetitive conditioning.
The amygdalae also are involved 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 assimilated into long-term storage over time (the duration of long-term memory storage can be life-long), 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 mice immediately after they learn something enhances their retention when they are tested two days later.
The amygdalae, especially the basolateral nuclei, are involved 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 classical conditioning 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 amygdalae is injected into the amygdalae, the animals had better memory for the training in the task. If a drug that inactivates the amygdalae is injected, the animals had impaired memory for the task.
Despite the importance of the amygdalae in modulating memory consolidation, however, learning can occur without it, though such learning appears to be impaired, as in fear conditioning impairments following amygdalar damage.
Buddhist monks who do compassion meditation have been shown to modulate their amygdala, along with their temporoparietal junction and insula, during their practice.
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 amygdalar activity, and that activity correlates with retention.
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."
Neuropsychological correlates of amygdalar activity
Early research on primates provided explanations as to the functions of the amygdala, as well as a basis for further research. As early as 1888, rhesus monkeys with a lesioned temporal cortex (including the amygdala) were observed to have significant social and emotional deficits. 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. Later studies served to focus on the amygdala specifically, as the temporal cortex encompasses a broad set of brain structures, making it difficult to find which ones specifically may have correlated with certain symptoms. Monkey mothers who had amygdala damage showed a reduction in maternal behaviors towards their infants, often physically abusing or neglecting them. In 1981, researchers found that selective radio frequency lesions of the whole amygdala caused Klüver-Bucy Syndrome.
With advances in neuroimaging technology such as MRI, neuroscientists have made significant findings concerning the amygdala in the human brain. Consensus of data shows the amygdala has a substantial role in mental states, and is related to many psychological disorders. 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. Individuals with psychopathy show reduced autonomic responses, relative to comparison individuals, to instructed fear cues. 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. 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 went on antidepressants. By contrast, the amygdala has been observed to relate 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. Many studies have focused on the connections between the amygdala and autism. Additional studies have shown a link between the amygdala and schizophrenia, noting that the right amygdala is significantly larger than the left in schizophrenic patients.
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. 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.
Recent research suggests that parasites, in particular toxoplasma, form cysts in the brain of rats, often taking up residence in the amygdala. This may provide clues as to how specific parasites may contribute to the development of disorders, including paranoia.