Fig. 10.

Simulations of amygdala lesions demonstrate that the amygdala is required for optimal acquisition but not for successful retention. (a) To simulate partial lesions of the amygdala before any training trials occur in delay conditioning (five training trials; unconditioned stimulus (US) onset at 550 ms, US duration = 50 ms, US offset at 600 ms, US level = 1), scalar β _A in the amygdala excitation term in Eq. 14 was progressively decreased. The results based on the conditioned stimulus (CS)-only presentation during retention testing are presented on a single graph of the variables for sensory cortex (S), orbitofrontal cortex (O), hippocampus (H), amygdala (A), hippocampal adaptive timing (R), and pontine nuclei (P): normal (solid line), 25 % decrease (dashed line), and 50 % decrease (dotted line). These graphs show a marker for the US presented in training for reference only (vertical dashed lines). The CS is also represented (vertical solid lines). Accurate conditioned response (CR) peak amplitude timing as measured by R remained consistent in all cases as in vivo but require additional training for improved responses (see Fig. 10b). The activity profiles of the pontine nuclei vary with the strength and timing of cortical activity to effect a CR. In vivo they are supplemented by learning in the cerebellum, where an adaptively-timed association is made between signals from the tone CS pathway from auditory nuclei to the pons, and from the pons via mossy fiber projections to the cerebellum, where they are trained by signals from the reflex US pathway from the trigeminal to inferior olive nuclei and then via climbing fibers to the cerebellum (Christian & Thompson, 2003; Fiala, Grossberg, & Bullock, 1996). (b) Simulation after ten delay conditioning training trials after partial lesions of the amygdala. All other input parameters and output variables are the same as in Fig. 10a. The CR peak amplitude improved as measured by R. Again, the activity profiles of the pontine nuclei vary with the strength and timing of cortical activity. (c) Simulation of partial lesions of the amygdala before any training trials occur in trace conditioning (20 training trials, US onset at 750 ms, US duration = 50 ms, US level = 1) show that both the CR amplitude and timing as measured by R and P are negatively impacted: normal (solid line), 25 % decrease (dashed line), and 50 % decrease (dotted line). The activity profiles of the pontine nuclei (P) reflect the experimental data that amygdala is important in trace conditioning. (d) Trace conditioning with amygdala (A) ablated 100 % after 20 acquisition trials but just before the retention test. On retention test with CS only, normal activity profiles for CS and US in sensory cortex (S) and orbitofrontal cortex (O) support normal adaptively-timed response in hippocampus (R), indicating a time-limited involvement of the amygdala during acquisition. The activity profile of the pontine nuclei (P) also supports the simulation of the data that amygdala involvement is time-limited