Fornix-fimbria section and working memory deficits in rats: Stimulus complexity and stimulus size.

Cassaday, Helen J.; Rawlins, J. N. P.

doi:10.1037/0735-7044.109.4.594

Cited by 44 publications

(60 citation statements)

References 38 publications

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“…Neither hippocampal nor fornix lesions affected DMS success except when the animals had to physically enter the goal. Control experiments showed that the problems animals had with enterable choices did not have to do with interference, complexity, or simplicity [26]. Similarly, early studies by Gaffan found that fornix lesions disrupted this sort of recognition memory in rats [56], but not in monkeys [57].…”

Section: Not All Cues Are Equalmentioning

confidence: 90%

“…And animal studies attempting to study recent declarative memory are inconsistent in their conclusions as to whether the hippocampus is involved in declarative memory or not [4,26,27 [4,26,27,32,45,70,113,119,133,135,137,253,257,258]. As with the water maze for spatial cognition, the DNMS task is a complex task that can be solved in a number of ways.…”

Section: Hmmentioning

confidence: 99%

“…Similarly, hippocampal lesions affect the radial and water mazes only when no direct cues are available. Cassaday and Rawlins [26,27] tested rats in a delayed-match-to-sample (DMS) task of choices between two goal boxes. Neither hippocampal nor fornix lesions affected DMS success except when the animals had to physically enter the goal.…”

Section: Not All Cues Are Equalmentioning

confidence: 99%

“…From the effect of hippocampal lesions, it is clear that the question of context is a complex one. For example, rats with hippocampal lesions can solve both simple and complex object-related DNMS tasks but they cannot differentiate long goal-boxes which they need to physically enter [26], see above.…”

Section: What's a Context?mentioning

confidence: 99%

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The hippocampal debate: are we asking the right questions?

Redish

2001

Behavioural Brain Research

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For years, the debate has been: 'Is the hippocampus the cognitive map?' or 'Is the hippocampus the core of memory?' These two hypotheses derived their original power from two key experiments-the cognitive map theory from the remarkable spatial correlates seen in recordings of hippocampal pyramidal cells and the memory theory from the profound amnesias seen in the patient H.M. Both of these key experiments have been reinterpreted over the years: hippocampal cells are correlated with much more than place and H.M. is missing much more than just his hippocampus. However, both theories are still debated today. The hippocampus clearly plays a role in both navigation and memory processing. The question that must be addressed is rather: 'What is the role played by the hippocampus in the navigation and memory systems?' By looking at the navigation system as a whole, one can identify the major role played by the hippocampus as correcting for accumulation errors that occur within idiothetic navigation systems. This is most clearly experimentally evident as reorientation when an animal is lost. Carrying this over to a more general process, this becomes a role of recalling a context, bridging a contextual gap, or, in other words, it becomes a form of recognition memory. I will review recent experimental data which seems to support this theory over the more general spatial or memory theories traditionally applied to hippocampus.

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Section: Not All Cues Are Equalmentioning

confidence: 90%

Section: Hmmentioning

confidence: 99%

Section: Not All Cues Are Equalmentioning

confidence: 99%

Section: What's a Context?mentioning

confidence: 99%

See 2 more Smart Citations

The hippocampal debate: are we asking the right questions?

Redish

2001

Behavioural Brain Research

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“…In one study, rats were given stimuli to recognize that were either small complex objects or much larger painted boxes (Warburton and Aggleton 1999). The rationale arose from evidence that rats with fornix lesions are selectively impaired with the latter (larger) stimuli (Cassaday and Rawlins 1995). Again, no lesion-induced deficit was found after anterior thalamic lesions.…”

Section: Anterior Thalamic Nucleimentioning

confidence: 99%

Unraveling the contributions of the diencephalon to recognition memory: A review

Aggleton¹,

Dumont²,

Warburton³

2011

Learn. Mem.

139

111

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Both clinical investigations and studies with animals reveal nuclei within the diencephalon that are vital for recognition memory (the judgment of prior occurrence). This review seeks to identify these nuclei and to consider why they might be important for recognition memory. Despite the lack of clinical cases with circumscribed pathology within the diencephalon and apparent species differences, convergent evidence from a variety of sources implicates a subgroup of medial diencephalic nuclei. It is supposed that the key functional interactions of this subgroup of diencephalic nuclei are with the medial temporal lobe, the prefrontal cortex, and with cingulate regions. In addition, some of the clinical evidence most readily supports dual-process models of recognition, which assume two independent cognitive processes (recollective-based and familiarity-based) that combine to direct recognition judgments. From this array of information a "multi-effect multinuclei" model is proposed, in which the mammillary bodies and the anterior thalamic nuclei are of preeminent importance for recollective-based recognition. The medial dorsal thalamic nucleus is thought to contribute to familiarity-based recognition, but this nucleus, along with various midline and intralaminar thalamic nuclei, is also assumed to have broader, indirect effects upon both recollective-based and familiarity-based recognition.Clinical studies repeatedly show that diencephalic pathology can impair recognition memory. Even so, there is no agreed locus within the diencephalon responsible for this memory loss and, hence, no agreed mechanism to explain the impairment. The present review examines both clinical and animal findings, and from this information a multi-effect multi-nuclei (MEMN) model emerges to explain the contributions of the diencephalon to recognition memory.At the outset, it is necessary to refine the focus of this review and to define some of its principal terms. The diencephalon comprises the thalamus and hypothalamus but, as will be explained, only the more medial parts of the diencephalon will be considered in detail. Recognition memory refers to the ability to detect whether a stimulus (e.g., a word, face, picture, object, or sound) has previously been encountered. As a consequence, this review is not about item identification (sometimes also confusingly referred to as recognition). Likewise, conditions that have broad disruptive effects on cognition, e.g., dementia, will not be considered even though recognition is typically impaired. Distinctions will be made between "item recognition," where the task is to determine if an individual item is novel or familiar, and "associative recognition," where all the individual items being experienced are familiar, but their particular combination is novel. A further, distinct ability is "recency" discrimination-the ability to determine which of two familiar stimuli has been experienced more recently. Both studies of amnesia and electrophysiological recordings show how recency memory and recogniti...

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Septohippocampal pathway as a site for the memory-impairing effects of ethanol

2000

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Ethanol affects behavior by interacting with synaptic sites at many levels of the nervous system. However, it targets most readily and at the lowest concentrations those sites mediating higher cognitive functions such as attention and memory. The memory‐impairing effects of ethanol are thought to involve the hippocampus, a structure particularly vulnerable to the effects ethanol at low concentrations and early in the rising phase of the blood ethanol concentration curve. One of the early, low‐dose effects of ethanol is an interruption of the normal physiological regulation of the hippocampus by the ascending septohippocampal pathway originating in the medial septal area (MSA). Ethanol enhances GABAergic transmission in the MSA, thereby reducing the regularity and vigor with which rhythmically bursting neurons of the MSA drive the hippocampal theta rhythm. Disruption of septohippocampal activity also has consequences on the response of the hippocampus to cortical inputs. Ethanol produces a loss of hippocampal responsivity that reduces the ability of the hippocampus to encode and retrieve relevant stimulus information necessary for accurate memory. This paper examines the behavioral and neural evidence for hippocampal vulnerability to ethanol and explores the hypothesis that these effects are due to ethanol disrupting septohippocampal modulation of the hippocampus, resulting in impairments of memory. Hippocampus 2000;10:111–121. © 2000 Wiley‐Liss, Inc.

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Fornix-fimbria section and working memory deficits in rats: Stimulus complexity and stimulus size.

Cited by 44 publications

References 38 publications

The hippocampal debate: are we asking the right questions?

The hippocampal debate: are we asking the right questions?

Unraveling the contributions of the diencephalon to recognition memory: A review

Septohippocampal pathway as a site for the memory-impairing effects of ethanol

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