- Basolateral amygdala (BLA)
- The lateral, basal, and accessory basal nuclei of the amygdala, collectively forming the main input region. The BLA receives sensory information from thalamus and cortex and is the site of fear conditioning — it is where conditioned stimulus-unconditioned stimulus associations are formed and stored via LTP-like plasticity. It projects to the central nucleus, which is the output hub.
- Central nucleus (CeA)
- The main output hub of the amygdala. Receives processed input from the BLA and projects to: the hypothalamus (triggering autonomic responses — elevated heart rate, sweating); the periaqueductal grey (PAG) in the brainstem (mediating freezing behaviour); and the HPA axis (triggering cortisol release via CRH). The CeA coordinates the full behavioural, autonomic, and endocrine fear response.
- Fear conditioning
- A form of classical conditioning in which a neutral conditioned stimulus (CS, e.g. a tone) is paired with an aversive unconditioned stimulus (US, e.g. a shock). After conditioning, the CS alone elicits a conditioned fear response — freezing, autonomic activation, cortisol release. The BLA is the critical site of CS-US association; lesioning it before or after conditioning prevents fear acquisition and expression respectively.
- Fear extinction
- The reduction of a conditioned fear response through repeated presentation of the CS without the US. Extinction does not erase the original fear memory but creates a new, competing inhibitory memory. The prefrontal cortex (vmPFC) plays a key role in encoding and expressing extinction memories; the amygdala stores both the original fear and the extinction memory. Context-dependence of extinction is why fear can return (renewal) when the context changes.
- Memory modulation hypothesis
- James McGaugh's hypothesis that the amygdala acts as a modulator of memory consolidation in other brain regions (primarily hippocampus). During emotionally arousing events, noradrenaline activates amygdala beta-adrenergic receptors, boosting its output to the hippocampus and entorhinal cortex. This enhances consolidation of the associated memory, producing the heightened vividness and durability of emotional memories. Propranolol (beta-blocker) given after a traumatic event can attenuate this enhancement.
- Klüver-Bucy syndrome
- A syndrome produced by bilateral temporal lobectomy in primates (first described by Klüver and Bucy, 1939) and by herpes simplex encephalitis in humans. Features include: emotional blunting/placidity (loss of normal fear and aggression responses), hypersexuality, hyperorality (tendency to examine all objects by mouth), and visual agnosia. The syndrome demonstrates the amygdala's role in emotional appraisal of stimuli.
- Patient SM
- A patient with bilateral amygdala calcification due to Urbach-Wiethe disease, studied by Feinstein, Adolphs, Damasio, and Tranel (2011). SM showed a specific inability to recognise fearful facial expressions, failed to generate skin conductance responses to aversive stimuli, and reported never experiencing subjective fear in objectively terrifying situations (snake rooms, haunted houses). SM's case demonstrates that the amygdala is necessary for both generating fear responses and the subjective experience of fear.