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S M Zola

Publications and source records attributed to S M Zola.

At least 19 recordsLinked to original sources
PubMed2001

Neuronal representations of stimulus associations develop in the temporal lobe during learning.

Visual stimuli that are frequently seen together become associated in long-term memory, such that the sight of one stimulus readily brings to mind the thought or image of the other. It has been hypothesized that acquisition of such long-term associative memories proceeds via the strengthening of connections between neurons representing the associated stimuli, such that a neuron initially responding only to one stimulus of an associated pair eventually comes to respond to both. Consistent with this hypothesis, studies have demonstrated that individual neurons in the primate inferior temporal cortex tend to exhibit similar responses to pairs of visual stimuli that have become behaviorally associated. In the present study, we investigated the role of these areas in the formation of conditional visual associations by monitoring the responses of individual neurons during the learning of new stimulus pairs. We found that many neurons in both area TE and perirhinal cortex came to elicit more similar neuronal responses to paired stimuli as learning proceeded. Moreover, these neuronal response changes were learning-dependent and proceeded with an average time course that paralleled learning. This experience-dependent plasticity of sensory representations in the cerebral cortex may underlie the learning of associations between objects.

Animals↗
PubMed2001

Relationship between magnitude of damage to the hippocampus and impaired recognition memory in monkeys.

Two recent meta-analyses, drawing on data from many of the same studies with monkeys, reached different conclusions about the relationship between hippocampal damage and recognition memory performance. Both studies found evidence of recognition memory impairment following hippocampal damage. However, Zola et al. (J Neurosci 2000;20:451-463) found no significant correlation between extent of hippocampal damage and recognition memory performance, whereas Baxter and Murray (Hippocampus 2001;11:61-71) concluded that the extent of hippocampal damage in monkeys was inversely correlated with impaired performance. Here, we first consider the requirements for carrying out a valid meta-analysis, and point out that the analysis carried out by Baxter and Murray (Hippocampus 2001;11:61-71) is invalid on simple statistical grounds. We then adopt the appropriate statistical procedures (multiple regression analyses rather than simple correlational analysis) to assess the relationship between extent of hippocampal damage and recognition performance across different studies. None of these analyses, including a reanalysis of the data of Baxter and Murray (Hippocampus 2001;11:61-71), revealed a significant inverse relationship between lesion size and behavioral impairment. Most of the variance was explained by differences between the studies that contributed to the meta-analysis, not by lesion size itself. Indeed, analysis of covariance indicated that there were differences among the studies beyond lesion size that significantly affected performance. Finally, we consider what relationship might hold between lesion size and memory performance in the monkey.

Animals↗
PubMed2001

Rats with lesions of the hippocampus are impaired on the delayed nonmatching-to-sample task.

Rats with ibotenic acid lesions of the hippocampus (H-IBO) were trained on the trial-unique delayed nonmatching-to-sample task (DNMS) using a short delay of 4 s. The H-IBO group learned the nonmatching rule as quickly as control animals. However, performance was impaired on the DNMS task when the delay between the sample and choice phase was increased to 1 or 2 min. The use of 4-s delay (probe) trials indicated that the H-IBO animals retained the nonmatching-to-sample rule throughout testing. In a second experiment, using the same groups of rats, extended training at the 1-min delay did not ameliorate the deficit produced by H-IBO lesions. The finding of impaired recognition memory in rats after hippocampal lesions is consistent with findings from humans and monkeys. Several methodological issues are considered that have complicated the interpretation of earlier studies of recognition memory in rats following hippocampal lesions. The capacity for recognition memory in humans, monkeys, and rodents is discussed as a straightforward example of hippocampus-dependent (declarative) memory.

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PubMed2000

Impaired recognition memory in rats after damage to the hippocampus.

Rats with radio-frequency or ibotenic acid lesions of the hippocampus and rats with radio-frequency lesions of the fornix were tested on the visual paired comparison task (VPC), a test of recognition memory. Memory was assessed at five different delay intervals ranging from 10 sec to 24 hr. All operated groups performed normally at the shorter delays (10 sec and 1 min). Across longer delays, the two groups with hippocampal damage were impaired. Rats with fornix lesions performed well on the VPC task but were impaired on a spatial task (spontaneous alternation). The results show that the hippocampus is essential for normal recognition memory. Moreover, fornix lesions need not mimic the effects of direct damage to hippocampal tissue. The findings are discussed in the context of the contribution of the hippocampus to recognition memory.

Animals↗
PubMed2000

Contrasting effects on discrimination learning after hippocampal lesions and conjoint hippocampal-caudate lesions in monkeys.

Eighteen monkeys with lesions of the hippocampal region (the hippocampus proper, the dentate gyrus, and the subiculum) made by an ischemic procedure, radio frequency, or ibotenic acid were tested on a simple, two-choice object discrimination learning task that has been shown to be sensitive to large lesions of the medial temporal lobe. The monkeys were also tested on two other discrimination tasks (pattern discrimination and eight-pair concurrent discrimination) that can be learned normally by monkeys with large medial temporal lobe lesions. All of the lesion groups were impaired at learning the simple object discrimination task. Seven of the monkeys who had sustained damage to the hippocampal region also sustained damage to the tail of the caudate nucleus. These seven monkeys, but not the other 11 monkeys with hippocampal lesions, were impaired on pattern discrimination and concurrent discrimination learning. The results suggest that the hippocampal region is important for learning easy, two-choice discriminations, whereas the caudate nucleus is necessary for the normal learning of more difficult, gradually acquired discrimination tasks. The findings support the distinction between declarative memory, which depends on the hippocampus and related medial temporal lobe structures, and habit learning, which depends on the caudate nucleus.

Animals↗
PubMed2000

Impaired recognition memory in monkeys after damage limited to the hippocampal region.

Monkeys with lesions limited to the hippocampal region (the hippocampus proper, the dentate gyrus, and the subiculum) were impaired on two tasks of recognition memory: delayed nonmatching to sample and the visual paired-comparison task. Recognition memory was impaired in five different groups of monkeys, whether the lesions were made by an ischemic procedure, by radio frequency, or by ibotenic acid. The finding that the hippocampal region is essential for normal recognition memory performance is considered in the context of current ideas about the role of the hippocampus in declarative memory.

Animals↗
PubMed1998

Episodic memory, semantic memory, and amnesia.

Episodic memory and semantic memory are two types of declarative memory. There have been two principal views about how this distinction might be reflected in the organization of memory functions in the brain. One view, that episodic memory and semantic memory are both dependent on the integrity of medial temporal lobe and midline diencephalic structures, predicts that amnesic patients with medial temporal lobe/diencephalic damage should be proportionately impaired in both episodic and semantic memory. An alternative view is that the capacity for semantic memory is spared, or partially spared, in amnesia relative to episodic memory ability. This article reviews two kinds of relevant data: 1) case studies where amnesia has occurred early in childhood, before much of an individual's semantic knowledge has been acquired, and 2) experimental studies with amnesic patients of fact and event learning, remembering and knowing, and remote memory. The data provide no compelling support for the view that episodic and semantic memory are affected differently in medial temporal lobe/diencephalic amnesia. However, episodic and semantic memory may be dissociable in those amnesic patients who additionally have severe frontal lobe damage.

Amnesia↗
PubMed1998

Memory, amnesia, and the issue of recovered memory: neurobiological aspects.

The main thesis of this article is that the debate about the credibility of "recovered memories"--reports by adults of recovered memories of childhood sexual abuse and trauma that were allegedly repressed for many years--can be usefully informed by considering the biological and behavioral facts and ideas about how memory works. Accordingly, the first section of this review describes current facts and ideas about the neurobiology and neuropsychology of memory and amnesia, including what parts of the brain are important for memory, distinctions between different memory systems in the brain, and the phenomena of infantile amnesia and source amnesia. The second section takes into account the information about the biological and behavioral bases of memory and addresses two questions about memory that have become a focus of debate in the recovered memory controversy, that is, whether memories for traumatic events change over time, and whether memories can be created for traumatic events that did not actually happen.

Adult↗
PubMed1998

A reexamination of the concurrent discrimination learning task: the importance of anterior inferotemporal cortex, area TE.

For 30 years, the concurrent discrimination learning task has figured prominently in studies used to determine the effects of medial temporal lobe damage in monkeys. However, the findings from these studies have been contradictory. We explored the contribution to concurrent discrimination performance of inadvertent damage to area TE by reexamining the behavioral data and histological material from monkeys with medial temporal lobe lesions previously tested in our laboratory. The amount of inadvertent damage to area TE was more predictive of impaired performance on the concurrent discrimination learning task than was the amount of damage to any medial temporal lobe structure, including the perirhinal cortex. These findings resolve earlier inconsistent findings regarding the concurrent discrimination learning task by demonstrating that performance on this task depends on area TE and not on perirhinal cortex or other medial temporal lobe structures.

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PubMed1997

Amnesia, memory and brain systems.

Bilateral damage to either the medial temporal lobe or the diencephalic midline causes an amnesic syndrome, i.e. a global impairment in the ability to acquire new memories regardless of sensory modality, and a loss of some memories, especially recent ones, from the period before amnesia began. The memory deficit can occur against a background of intact intellectual and perceptual functions. Two themes have been prominent in recent work. First, the amnesic syndrome is narrower than once believed in the sense that a number of learning and memory abilities are preserved (e.g. skill and habit learning, simple forms of conditioning and the phenomenon of priming). Second, the brain system damaged in amnesia has only a temporary role in memory. As time passes after learning, memory is reorganized and consolidated within neocortex, such that eventually medial temporal lobe and diencephalic structures are not needed for storage or retrieval.

Amnesia↗
PubMed1997

The neurobiology of recovery memory.

The so-called recovery memory syndrome--reports by adults of recovered memories of childhood sexual abuse and trauma that were allegedly "repressed" for many years--has become an important issue in the field of mental health. In particular, there is debate about the credibility of recovered memories. The author describes findings in several fields of brain science about the way memory works and how memory is organized in the brain. These findings clarify aspects of normal memory function and the process of memory distortion, and they provide a neurobiological perspective from which to approach the topic of recovered memory.

Adult↗
PubMed1996

Structure and function of declarative and nondeclarative memory systems.

This article reviews recent studies of memory systems in humans and nonhuman primates. Three major conclusions from recent work are that (i) the capacity for nondeclarative (nonconscious) learning can now be studied in a broad array of tasks that assess classification learning, perceptuomotor skill learning, artificial grammar learning, and prototype abstraction; (ii) cortical areas adjacent to the hippocampal formation, including entorhinal, perirhinal, and parahippocampal cortices, are an essential part of the medial temporal lobe memory system that supports declarative (conscious) memory; and (iii) in humans, bilateral damage limited to the hippocampal formation is nevertheless sufficient to produce severe anterograde amnesia and temporally graded retrograde amnesia covering as much as 25 years.

Amnesia↗
PubMed1996

Three cases of enduring memory impairment after bilateral damage limited to the hippocampal formation.

Patient RB (Human amnesia and the medial temporal region: enduring memory impairment following a bilateral lesion limited to field CA1 of the hippocampus, S. Zola-Morgan, L. R. Squire, and D. G. Amaral, 1986, J Neurosci 6:2950-2967) was the first reported case of human amnesia in which detailed neuropsychological analyses and detailed postmortem neuropathological analyses demonstrated that damage limited to the hippocampal formation was sufficient to produce anterograde memory impairment. Neuropsychological and postmortem neuropathological findings are described here for three additional amnesic patients with bilateral damage limited to the hippocampal formation. Findings from these patients, taken together with the findings from patient RB and other amnesic patients, make three important points about memory. (1) Bilateral damage limited primarily to the CA1 region of the hippocampal formation is sufficient to produce moderately severe anterograde memory impairment. (2) Bilateral damage beyond, the CA1 region, but still limited to the hippocampal formation, can produce more severe anterograde memory impairment. (3) Extensive, temporally graded retrograde amnesia covering 15 years or more can occur after damage limited to the hippocampal formation. Findings from studies with experimental animals are consistent with the findings from amnesic patients. The present results substantiate the idea that severity of memory impairment is dependent on locus and extent of damage within the hippocampal formation and that damage to the hippocampal formation can cause temporally graded retrograde amnesia.

Aged↗
PubMed1996

Ischemic brain damage and memory impairment: a commentary.

Studies in humans and monkeys have identified structures in the medial temporal lobe essential for memory (the hippocampal region, i.e., the dentate gyrus, the hippocampus, and the subicular complex, and the adjacent perirhinal, entorhinal, and parahippocampal cortices). Additional work has revealed that for both species, damage limited to the hippocampal region produces less severe memory impairment than damage that includes additional structures within the medial temporal lobe. This work has been based on both neurosurgical lesions and on lesions produced by global ischemia or anoxia. An important issue about ischemic damage is whether the damage identifiable in histopathological examination provides an accurate estimate of direct neural damage or whether additional direct damage might be present that is sufficient to disrupt neuronal function in areas important for memory and sufficient to impair behavioral performance, but not sufficient to progress to cell death and to be detectable in conventional histopathology. This commentary explores the issue of ischemic damage and memory impairment. Although few studies have addressed this issue directly, the currently available data from global ischemia in rats, monkeys, and humans are consistent with the hypothesis that the detectable neuronal damage is responsible for the severity of the observed behavioral impairment. Yet it is also true that this hypothesis has not been the target of very much systematic work. We encourage additional experimental work, especially in rats, that could further illuminate how to evaluate the behavioral effects of ischemic lesions.

Amnesia↗
PubMed1996

Memory, memory impairment, and the medial temporal lobe.

The cognitive and neuroanatomical work described here should be viewed as a first step in analyzing how the brain has organized its memory functions, which can open the door to more detailed neurobiological analysis. With respect to declarative memory, it should soon be possible to study representations directly in neocortex with the technique of single-cell recording, to observe directly the development of neuronal plasticity important for declarative memory, and to determine how the medial temporal lobe interacts with neocortex during learning, consolidation, and retrieval. In this regard, the paradigms developed by Miyashita and his colleagues appear to hold particular promise (Sakai and Miyashita 1991; Higuchi and Miyashita 1996). With respect to nondeclarative memory, it is now possible to identify particular brain systems that are essential for particular kinds of memory. An important next step will be to determine whether these systems are essential for the acquisition, storage, or expression of memory, and to identify exactly where the synaptic changes occur that support each kind of memory.

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PubMedDate not supplied

Perception and recognition memory in monkeys following lesions of area TE and perirhinal cortex.

Monkeys with lesions of perirhinal cortex (PR group) and monkeys with lesions of inferotemporal cortical area TE (TE group) were tested on a modified version of the delayed nonmatching to sample (DNMS) task that included very short delay intervals (0.5 sec) as well as longer delay intervals (1 min and 10 min). Lesions of the perirhinal cortex and lesions of area TE produced different patterns of impairment. The PR group learned the DNMS task as quickly as normal monkeys (N) when the delay between sample and choice was very short (0.5 sec). However, performance of the PR group, unlike that of the N group, fell to chance levels when the delay between sample and choice was lengthened to 10 min. In contrast to the PR group, the TE group was markedly impaired on the DNMS task even at the 0.5-sec delay, and three of four monkeys with TE lesions failed to acquire the task. The results provide support for the idea that perirhinal cortex is important not for perceptual processing, but for the formation and maintenance of long-term memory. Area TE is important for the perceptual processing of visual stimuli.

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