A rat is fear-conditioned: tone (CS) paired with foot shock (US). After conditioning, the tone alone causes freezing. The rat's central amygdala is then lesioned. What would you predict?
AThe rat shows no fear response at all — the learned association is destroyed along with the expression circuit
BThe rat still learns new fear associations but can no longer express the defensive responses (freezing, heart rate increase) to previously learned cues
CThe lesion has no effect because fear expression is entirely mediated by the lateral amygdala
DThe rat becomes hyperaggressive because fear suppression circuits are removed
The lateral amygdala is the learning site — the tone-shock association is stored there via LTP. The central amygdala is the output hub, projecting to the hypothalamus (stress hormones), periaqueductal gray (freezing), and brainstem autonomic nuclei (heart rate). Lesioning the central amygdala disconnects stored associations from their expression — the rat 'knows' to fear the tone but cannot express the behavioral and physiological responses. This is the classic dissociation between fear acquisition (lateral) and fear expression (central).
Question 2 Multiple Choice
Why does elevated dopamine during an emotionally significant event make the resulting memory more durable?
ADopamine directly activates sensory cortex, making perceptual encoding sharper during arousing events
BDopamine signals motivational salience and modulates consolidation in the basolateral amygdala, strengthening the synaptic changes underlying the memory
CDopamine inhibits the hippocampus during emotional events, preventing interference from competing contextual memories
DDopamine is the primary neurotransmitter for fear learning; without it, lateral amygdala LTP cannot occur at all
Dopaminergic input to the basolateral amygdala (BLA) modulates consolidation — the post-encoding stabilization of newly formed synaptic changes. When dopamine is elevated (signaling that an event is salient), BLA neurons consolidate the memory trace more robustly, producing more durable long-term storage. This is adaptive: survival-relevant events (predators, food sources, social threats) are encoded with high fidelity. The same mechanism explains why traumatic experiences form especially strong, sometimes overgeneralized memories — a vulnerability relevant to PTSD.
Question 3 True / False
The amygdala forms fear associations using long-term potentiation (LTP) — the same synaptic plasticity mechanism that underlies memory formation in the hippocampus.
TTrue
FFalse
Answer: True
The lateral amygdala uses Hebbian LTP to associate conditioned stimuli with unconditioned stimuli: when the tone input and the shock input arrive simultaneously, their synaptic co-activation strengthens the tone pathway via LTP, so the tone alone can subsequently drive the circuit. This is the same cellular mechanism studied in hippocampal place cells and long-term memory. The amygdala is not a fundamentally different type of memory system; it is the same molecular machinery embedded in a circuit specialized for emotionally significant, survival-relevant learning.
Question 4 True / False
Lesioning the lateral amygdala would eliminate the physical expression of fear responses (freezing, heart rate increase) while leaving the learned fear association itself intact.
TTrue
FFalse
Answer: False
This reverses the roles of the two amygdala subdivisions. The lateral amygdala is the acquisition and storage site — the learned CS-US association is encoded there via LTP. Lesioning the lateral amygdala destroys the stored association, leaving no fear to express. The central amygdala is the output hub; a central amygdala lesion would preserve the stored association but disconnect it from expression. Confusing these two roles is the most common error when students are first learning amygdala circuitry.
Question 5 Short Answer
Explain the functional division of labor between the lateral and central amygdala in fear conditioning, and why this distinction matters for understanding anxiety disorders.
Think about your answer, then reveal below.
Model answer: The lateral amygdala is the input and learning site: it receives convergent sensory information about the conditioned stimulus and the aversive unconditioned stimulus, and LTP at these synapses encodes the learned association. The central amygdala is the output hub: it receives from the lateral amygdala and projects to downstream structures (hypothalamus, PAG, brainstem) that generate the behavioral and physiological fear responses. These are dissociable processes. In anxiety disorders, the lateral amygdala may form associations too readily (fear conditioning with minimal trauma), generalize too broadly (neutral cues trigger responses), or produce associations too resistant to extinction. Effective treatments like exposure therapy drive extinction learning — new synaptic changes in the lateral amygdala that compete with the original fear memory — rather than suppressing the central amygdala's output.
Understanding this circuit division reveals that fear learning and fear expression are separate and dissociable, which has direct implications for where therapeutic interventions act and why they succeed or fail.