There is considerable evidence that the hippocampal system contributes both to (1) the temporary maintenance of memories and to (2) the processing of a particular type of memory representation. The findings on amnesia suggest that these two distinguishing features of hippocampal memory processing are orthogonal. Together with anatomical and physiological data, the •neuropsychological findings support a model of cortico-hippocampal interactions in which the temporal and representational properties of hippocampal memory processing are mediated separately. We propose that neocortical association areas maintain shortterm memories for specific items and events prior to hippocampal processing as well as providing the final repositories of long-term memory. The parahippocampal region supports intermediate-term storage of individual items, and the hippocampal formation itself mediates an organization of memories according to relevant relationships among items. Hippocampal-cortical interactions produce (i) strong and persistent memories for events, including their constituent elements and the relationships among them, and (ii) a capacity to express memories flexibly across a wide range of circumstances.It has been known for decades that the hippocampal system plays a prominent role in learning and memory. Only recently has it become clear that only certain properties of memory processing depend on hippocampal system function and that these can be distinguished operationally from other aspects of memory that do not. It has proved difficult, however, to arrive at an understanding of memory rich enough to characterize both the nature of memory that is dependent on the hippocampal system and memory that is independent of this processing, and to tie them to underlying neural mechanisms. The earliest reports of amnesia emphasized the timelimited role of the hippocampal region in memory, focusing on its critical function in "consolidation" processes that bridge between immediate memory and the longterm store (Scoville & Milner 1957). This temporal distinction is most striking: amnesic patients and animals with hippocampal system damage show normal retention at short delays and increasingly impaired retention with longer delays. Recently, some have argued that virtually all aspects of memory processing by the hippocampal system can be attributed to its function as a temporary memory store or buffer (e.g., Rawlins 1985). However, a large body of data indicates that the loss of consolidation or memory-buffer functions cannot account for the full pattern of impaired and spared memory performance observed after hippocampal system damage; some memory capacities are intact in amnesia even across very long temporal intervals, whereas other aspects of memory performance are grossly impaired even over relatively short retention intervals. The buffer hypothesis also fails to account fully for a number of relevant observations on the stable, long-lasting functional correlates of hippocampal neuronal activity (see sect. 5). To accommodate a ...
The activity of 378 single neurons was recorded from areas of the parahippocampal region (PHR), including the perirhinal and lateral entorhinal cortex, as well as the subiculum, in rats performing an odor-guided delayed nonmatching-to-sample task. Nearly every neuron fired in association with some trial event, and every identifiable trial event or behavior was encoded by neuronal activity in the PHR. The greatest proportion of cells was active during odor sampling, and for many cells, activity during this period was odor selective. In addition, odor memory coding was reflected in two general ways. First, a substantial proportion of cells showed odorselective activity throughout or at the end of the memory delay period. Second, odor-responsive cells showed odor-selective enhancement or suppression of activity during stimulus repetition in the recognition phase of the task. These data, combined with evidence that the PHR is critical for maintaining odor memories in animals performing the same task, indicate that this cortical region mediates the encoding of specific memory cues, maintains stimulus representations, and supports specific match-nonmatch judgments critical to recognition memory. By contrast, hippocampal neurons do not demonstrate evoked or maintained stimulusspecific codings, and hippocampal damage results in little if any decrement in performance on this task. Thus it becomes increasingly clear that the parahippocampal cortex can support recognition memory independent of the distinct memory functions of the hippocampus itself. Key words: entorhinal cortex; perirhinal cortex; subiculum; hippocampus; recognition memory; delayed nonmatching; single unitsThe parahippocampal region (PHR) has become a focus for anatomical, behavioral, and electrophysiological studies of the medial temporal lobe memory system (Eichenbaum et al., 1994;Brown, 1996;Murray, 1996;Suzuki, 1996). This cortical area surrounds the hippocampus and amygdala and is composed of several distinct subdivisions, including the perirhinal, entorhinal, and parahippocampal (in monkeys) or postrhinal (in rats) cortices (Witter et al., 1989;Burwell et al., 1995). The PHR receives inputs from widespread secondary or "association" cortical regions and provides the major conduit for hippocampal outputs to the same cortical association areas. This anatomical evidence indicates that the PHR occupies a pivotal position for mediating memory functions of the hippocampal region.Neuropsychological findings indicate that the PHR indeed plays a critical role in recognition memory, independent of its role as an intermediary for cortical-hippocampal interactions (Eichenbaum et al., 1994;Murray, 1996). This evidence comes mainly from experiments examining the effects of damage to the hippocampal region on performance in a simple recognition memory test known as delayed nonmatching to sample (DNMS) (Eichenbaum et al., 1994). In the standard version of this task, originally devised by Gaffan (1974), animals are presented with a novel "sample" cue and then after a...
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.
The rapid encoding of contextual memory requires the CA3 region of hippocampus, but the necessary genetic pathways remain unclear. We found that the activity-dependent transcription factor Npas4 regulates a transcriptional program in CA3 that is required for contextual memory formation. Npas4 was specifically expressed in CA3 after contextual learning. Global knockout or selective deletion of Npas4 in CA3 both resulted in impaired contextual memory, and restoration of Npas4 in CA3 was sufficient to reverse the deficit in global knockout mice. By recruiting RNA polymerase II to promoters and enhancers of target genes, Npas4 regulates a learning-specific transcriptional program in CA3 that includes many well-known activity-regulated genes, suggesting that Npas4 is a master regulator of activity-regulated gene programs and is central to memory formation.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.