Olfaction is the only sense that bypasses the thalamus. Two to three synapses separate the nose from the amygdala and hippocampus.
Fear conditioning doesn't only update cortex. Glomeruli in the olfactory bulb that process the conditioned odor enlarge. Receptor neuron populations expand. The amygdala projects centrifugal feedback back to the olfactory bulb, allowing emotional state to modify sensory processing before the signal leaves the primary structure. The structural change reverses during extinction. The sensor carries the organism's history.
receptor neurons
→ piriform cortex
The enlarged glomerulus modifies the signal before it reaches any cortical area involved in identifying or naming what you're smelling. The evaluation may run before the identification is available. What the simulation cannot show: whether this peripheral change alters the subjective quality of encountering the feared odor — the phenomenology from inside — or whether the lived texture of the smell remains constant while only the response changes downstream.
It also can't show the molecular mechanism: BDNF signaling, neurogenesis in the olfactory epithelium, receptor neuron proliferation over days of repeated exposure. The size change here is measured in display units. The biological change accumulates over time, involves cell population dynamics, and is not triggered by single trials.