Temporal discrimination learning in severe amnesic patients reveals an alteration in the timing of eyeblink conditioned responses.

This study investigated whether the hippocampal system plays a modulatory role in the timing of conditioned responses (CRs) in eyeblink classical conditioning. Seven bitemporal amnesic patients and 7 controls were randomly presented 2 tone conditioned stimuli (CSs) that were individually paired with two different interstimulus intervals (ISIs) in a delay conditioning task. It was found that amnesic patients' CRs occurred significantly earlier than control participants' CRs at the longer ISI. Amnesic patients also produced significantly more nonadaptive CRs than did control participants, their level of acquisition was less than that of control participants after equating for ISI, and they did not show extinction with the longer ISI. These data suggest a role of the hippocampal system in controlling the precise timing of conditioned eyeblink responses and in acquiring and extinguishing responses within the context of a temporal discrimination task.

Impaired trace eyeblink conditioning in bilateral, medial-temporal lobe amnesia.

Trace eyeblink classical conditioning was assessed in patients with bilateral medial-temporal amnesia and matched control participants who had previously shown equivalent delay eyeblink conditioning (J. D. E. Gabrieli et al., 1995). The silent trace interval varied for durations of 500, 750, or 1,000 ms in successive sessions separated by at least 2 weeks; extinction trials followed each session. Patients with amnesia produced significantly fewer conditioned responses (CRs) than did control participants at all trace intervals. Both groups produced fewer CRs as the trace interval lengthened. Thus, the temporal lobe memory system in humans makes an essential contribution to normal acquisition in trace, but not delay, classical eyeblink conditioning.

Latent learning in medial temporal amnesia: evidence for disrupted representational but preserved attentional processes.

Damage to the hippocampus and medial temporal (MT) structures can lead to anterograde amnesia and may also impair latent learning, in which prior exposure to cues affects their subsequent associability. Normally, latent learning may reflect both representational and attentional mechanisms. Prior work has suggested that individuals with MT amnesia have specific deficits in representational processing; thus, latent learning that invokes primarily representational mechanisms might be especially impaired in MT amnesia. The current results provide preliminary confirmation of this prediction. In Experiment 1, a latent learning paradigm expected to invoke representational mechanisms was impaired in individuals with MT amnesia, whereas in Experiment 2, a paradigm expected to invoke other attentional mechanisms was spared in individuals with MT amnesia. This suggests the representational and attentional components of latent learning are dissociable and differentially affected in anterograde amnesia.