Complementary roles of the orbital prefrontal cortex and the perirhinal-entorhinal cortices in an odor-guided delayed-nonmatching-to-sample task.

Abstract

Continuing efforts toward designing odor-guided tasks for rats that are similar in memory demands to tasks used typically with primates have resulted in the development of a continuous delayed-nonmatching-to-sample (cDNM) task that is guided by olfactory stimuli. The results indicate that normal subjects acquire the cDNM task rapidly and that subsequent performance deteriorates with increases in memory delay or interitem interference. Moreover, different aspects of cDNM performance were shown to be differentially sensitive to selective lesions of the orbitofrontal and parahippocampal areas. Orbitofrontal cortex lesions disproportionately impaired cDNM acquisition; delay performance was impaired only under conditions of elevated levels of interitem interference. Combined perirhinal and entorhinal cortical lesions had no effect on cDNM acquisition but impaired cDNM performance at longer delays across all levels of interference. Fornix lesions did not impair either acquisition of cDNM or subsequent performance across long delays and increased interference. This pattern of impaired and spared capacities is similar to that observed in monkeys after lesions of analogous areas and is consistent with the notion that the prefrontal cortical system contributes preferentially to learning general task "rules" such as the nonmatching rule that is inherent in cDNM, whereas the perirhinal and entorhinal cortical areas are involved in the intermediate-term maintenance of memories for specific information.

Neurobiological foundations of an attribute model of memory

“…Supporting evidence is based on the findings that lesions of the AI/LO cortex produce deficits in working memory for affect based on taste or odor information (DeCoteau et al, 1997;Di Pietro et al, 2004;Otto & Eichenbaum, 1992;Ragozzino & Kesner, 1999). Further support can be found in a study where sustained neuronal firing was observed in the AI/LO cortex during the delay period in a non-matching-to-sample for odors task (Ramus & Eichenbaum, 2000).…”

“…Based on the empirical findings that all sensory inputs are processed by the DG subregion of the hippocampus ( (Aggleton, Hunt, & Rawlins, 1986;Jackson-Smith et al, 1993;Kesner et al, 1993;Mumby, Wood, & Pinel, 1992;Otto & Eichenbaum, 1992), it has been suggested that a possible role for the hippocampus might be to provide for sensory markers to demarcate a spatial location, so that the hippocampus can more efficiently mediate spatial information. It is thus possible that one of the main process functions of the hippocampus is to encode and separate spatial events from each other.…”

The Temporal Context Model in Spatial Navigation and Relational Learning: Toward a Common Explanation of Medial Temporal Lobe Function Across Domains.

“…Suzuki, Miller, and Desimone (1997) extended this result to demonstrate that this stimulus-specific firing persisted across multiple intervening stimuli. Buffalo, Reber, and Squire (1998) showed that people with lesions to the perirhinal cortex showed deficits of recognition memory over delays as short as 6 s. Mumby and Pinel (1994) showed that rats with damage to entorhinal and perirhinal cortex were impaired on delayed non-match to sample (DNMS) of trial-unique object at delays as short as 15 s. Otto and Eichenbaum (1992) showed no deficit in a continuous delayed non-match task from fornix transection, but showed a deficit from combined perirhinal/entorhinal lesions at delays of 30 s. This not only points to a role for the parahippocampal regions in memory on the time scale of the recency effect in free recall, but argues against a role of the hippocampus in such processes. Murray and Mishkin (1998), showed that lesions to the amygdala and hippocampus that spared rhinal cortex did not have an effect on DNMS performance, whereas a comparable study showed a severe impairment from rhinal cortex lesions at delays as short as tens of seconds (Meunier, Bachevalier, Mishkin, & Murray, 1993 The first suggestion comes from the finding that hippocampal damage is associated with a disruption of memory for items from the early part of the serial position curve.…”

Topographic organization of the reciprocal connections between the monkey entorhinal cortex and the perirhinal and parahippocampal cortices

“…Given the important role of the entorhinal, perirhinal, and parahippocampal cortices in conveying sensory information to and from the hippocampal formation, it is not surprising that damage to these regions produces a memory impairment in monkeys (Murray and Mishkin, 1986;Zola-Morgan et al, 1989b;Gaffan and Murray, 1992;Suzuki et al, 1993) and rats (Otto and Eichenbaum, 1992). In monkeys, bilateral lesions limited to the perirhinal and parahippocampal cortices (the PRPH lesion) produce a severe anterograde memory impairment that resembles human amnesia.…”