title: The role of the hippocampus in trace conditioning: temporal discontinuity or task difficulty?
abstract: It is well established that the hippocampal formation is critically involved in the acquisition of trace memories, a paradigm in which the conditioned (CS) and unconditioned stimuli (US) are separated by a temporal gap (Solomon et al., 1986). The structure is reportedly not critical for the acquisition of delay memories, where the CS and the US overlap in time (Berger & Orr, 1983; Schmaltz & Theios, 1972). Based on these results, it is often stated that the hippocampus is involved in "filling the gap" or otherwise associating the two stimuli in time. However, in addition to the presence of a temporal gap, there are other differences between trace and delay conditioning. The most apparent difference is that animals require many more trials to learn the trace task, and thus it is inherently more difficult than the delay task. Here, we tested whether the hippocampus was critically involved in delay conditioning, if it was rendered more difficult such that the rate of acquisition was shifted to be analogous to trace conditioning. Groups of rats received excitotoxic lesions to the hippocampus, sham lesions or were left intact. Using the same interstimulus intervals (ISI), control animals required more trials to acquire the trace than the delay task. As predicted, animals with hippocampal lesions were impaired during trace conditioning but not delay conditioning. However, when the delay task was rendered more difficult by extending the ISI (a long delay task), animals with hippocampal lesions were impaired. In addition, once the lesioned animal learned the association between the CS and the US during delay conditioning, it could learn and perform the trace CR. Thus, the role of the hippocampus in classical conditioning is not limited to learning about discontiguous events in time and space; rather the structure can become engaged simply as a function of task difficulty.
authors.affiliation: Department of Psychology and Program in Neuroscience, Princeton University, Princeton, New Jersey, USA.
authors.forename: A V
authors.initials: AV
authors.lastname: Beylin
authors.forename: C C
authors.initials: CC
authors.lastname: Gandhi
authors.forename: G E
authors.initials: GE
authors.lastname: Wood
authors.forename: A C
authors.initials: AC
authors.lastname: Talk
authors.forename: L D
authors.initials: LD
authors.lastname: Matzel
authors.forename: T J
authors.initials: TJ
authors.lastname: Shors
mesh_terms: D000818:Animals; D001245:Association Learning / Q000502:physiology; D003215:Conditioning, Eyelid / Q000502:physiology*; D006624:Hippocampus / Q000473:pathology / Q000502:physiology*; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors