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Larry R Squire - One of the best experts on this subject based on the ideXlab platform.
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When Recognition Memory is independent of hippocampal function
Proceedings of the National Academy of Sciences of the United States of America, 2014Co-Authors: Christine N. Smith, Annette Jeneson, Jennifer C. Frascino, C. Brock Kirwan, Ramona O. Hopkins, Larry R SquireAbstract:Hippocampal damage has been thought to result in broad Memory impairment. Recent studies in humans, however, have raised the possibility that Recognition Memory for faces might be spared. In five experiments we investigated face Recognition in patients with hippocampal lesions (H) or large medial temporal lobe (MTL) lesions, including patients where neurohistological information was available. Recognition of novel faces was unequivocally intact in H patients but only at a short retention interval. Recognition Memory for words, buildings, inverted faces, and famous faces was impaired. For MTL patients, Recognition Memory was impaired for all materials and across all retention intervals. These results indicate that structures other than the hippocampus, perhaps the perirhinal cortex, can support face Recognition Memory in H patients under some conditions. The fact that the faces were novel when Recognition Memory was intact does not fully account for our findings. We propose that the role of the hippocampus in Recognition Memory is related to how Recognition decisions are accomplished. In typical Recognition tasks, participants proceed by forming an association between a study item and the study list, and the Recognition decision is later made based on whether participants believe the item was on the study list. We suggest that face Recognition is an exception to this principle and that, at short retention intervals, participants can make their Recognition decisions without making explicit reference to the study list. Important features of faces that might make face Recognition exceptional are that they are processed holistically and are difficult to verbally label.
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object Recognition Memory and the rodent hippocampus
Learning & Memory, 2010Co-Authors: Nicola J Broadbent, Larry R Squire, Stephane Gaskin, Robert E. ClarkAbstract:Recognition Memory refers to the ability to judge a previously encountered item as familiar and depends on the integrity of the medial temporal lobe (Squire et al. 2007). Tasks that assess Recognition Memory (and object Recognition Memory in particular) have become increasingly useful tools for basic and preclinical research investigating the neural basis of Memory (Winters et al. 2008). Perhaps the best known of these tasks is the novel object Recognition task (NOR) (also known as the visual paired-comparison task in studies with humans and monkeys). Studies of the NOR task in humans with hippocampal damage (McKee and Squire 1993; Pascalis et al. 2004) and in monkeys with selective damage to the hippocampus (Pascalis and Bachevalier 1999; Zola et al. 2000; Nemanic et al. 2004) have resulted in clear and consistent findings. Damage limited to the hippocampus is sufficient to produce impaired Recognition Memory (Squire et al. 2007, Box 1). In rats and mice, the NOR task has become particularly popular and is currently a benchmark task for assessing Recognition Memory. Yet despite its widespread use in rodents, the findings are rather mixed. For example, in the rat, although there is agreement that the perirhinal cortex is critically important for normal NOR performance, there is less agreement about the hippocampus (for review, see Winters et al. 2008). Although some of the discrepancies between studies may be attributed to differences in lesion size and in the length of the retention delay (Broadbent et al. 2004), these factors cannot account for all the findings (Squire et al. 2007). Whereas most studies have investigated the effects of hippocampal lesions on postoperative NOR performance, there is also interest in the effects of hippocampal lesions on Memory for previously encountered objects. For a number of tasks, hippocampal lesions produce temporally graded retrograde amnesia, such that Memory acquired recently is impaired and Memory acquired more remotely is spared (for review, see Squire et al. 2004; Frankland and Bontempi 2005). In the case of the single study of retrograde Memory that has involved the NOR task, Recognition Memory was impaired when a 5-wk interval intervened between training and hippocampal surgery (Gaskin et al. 2003). It remains possible that Memory might be spared if a longer delay was imposed between training and surgery. The aim of the present study was to assess both the anterograde and retrograde effects of hippocampal lesions on Recognition Memory using the NOR task. To thoroughly assess the effects of hippocampal lesions we used (1) large groups of animals, (2) multiple tests of NOR Memory, (3) a scoring method that allowed object preference to be determined on a second-by-second basis during the Recognition tests, and (4) a novel training protocol that permitted the evaluation of Recognition Memory even after a retention interval as long as 10 wk.
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object Recognition Memory and the rodent hippocampus
Learning & Memory, 2010Co-Authors: Nicola J Broadbent, Larry R Squire, Stephane Gaskin, Robert E. ClarkAbstract:In rodents, the novel object Recognition task (NOR) has become a benchmark task for assessing Recognition Memory. Yet, despite its widespread use, a consensus has not developed about which brain structures are important for task performance. We assessed both the anterograde and retrograde effects of hippocampal lesions on performance in the NOR task. Rats received 12 5-min exposures to two identical objects and then received either bilateral lesions of the hippocampus or sham surgery 1 d, 4 wk, or 8 wk after the final exposure. On a retention test 2 wk after surgery, the 1-d and 4-wk hippocampal lesion groups exhibited impaired object Recognition Memory. In contrast, the 8-wk hippocampal lesion group performed similarly to controls, and both groups exhibited a preference for the novel object. These same rats were then given four postoperative tests using unique object pairs and a 3-h delay between the exposure phase and the test phase. Hippocampal lesions produced moderate and reliable Memory impairment. The results suggest that the hippocampus is important for object Recognition Memory.
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Impaired odor Recognition Memory in patients with hippocampal lesions.
Learning & memory (Cold Spring Harbor N.Y.), 2004Co-Authors: Daniel A. Levy, Ramona O. Hopkins, Larry R SquireAbstract:In humans, impaired Recognition Memory following lesions thought to be limited to the hippocampal region has been demonstrated for a wide variety of tasks. However, the importance of the human hippocampus for olfactory Recognition Memory has scarcely been explored. We evaluated the ability of Memory-impaired patients with damage thought to be limited to the hippocampal region to recognize a list of odors. The patients were significantly impaired after a retention delay of 1 h. Olfactory sensitivity was intact. This finding is in agreement with earlier reports that rats with hippocampal lesions exhibited Memory impairment on an odor delayed nonmatching to sample task (after 30 min and 1 h) and that patients with damage thought to be limited to the hippocampal region were impaired on an odor span Memory task. Olfactory Recognition Memory, similar to Recognition Memory in other sensory modalities, depends on the integrity of the hippocampal region.
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spatial Memory Recognition Memory and the hippocampus
Proceedings of the National Academy of Sciences of the United States of America, 2004Co-Authors: Nicola J Broadbent, Larry R Squire, Robert E. ClarkAbstract:There is wide agreement that spatial Memory is dependent on the integrity of the hippocampus, but the importance of the hippocampus for nonspatial tasks, including tasks of object Recognition Memory is not as clear. We examined the relationship between hippocampal lesion size and both spatial Memory and object Recognition Memory in rats. Spatial Memory was impaired after bilateral dorsal hippocampal lesions that encompassed 30-50% total volume, and as lesion size increased from 50% to ≈100% of total hippocampal volume, performance was similarly impaired. In contrast, object Recognition was intact after dorsal hippocampal lesions that damaged 50-75% of total hippocampal volume and was impaired only after larger lesions that encompassed 75-100% of hippocampal volume. Last, ventral hippocampal lesions that encompassed ≈50% of total hippocampal volume impaired spatial Memory but did not affect object Recognition Memory. These findings show that the hippocampus is important for both spatial Memory and Recognition Memory. However, spatial Memory performance requires more hippocampal tissue than does Recognition Memory.
Malcolm W. Brown - One of the best experts on this subject based on the ideXlab platform.
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Neural circuitry for rat Recognition Memory
Behavioural brain research, 2014Co-Authors: E C Warburton, Malcolm W. BrownAbstract:Information concerning the roles of different brain regions in Recognition Memory processes is reviewed. The review concentrates on findings from spontaneous Recognition Memory tasks performed by rats, including Memory for single objects, locations, object–location associations and temporal order. Particular emphasis is given to the potential roles of different regions in the circuit of interacting structures involving the perirhinal cortex, hippocampus, medial prefrontal cortex and medial dorsal thalamus in Recognition Memory for the association of objects and places. It is concluded that while all structures in this circuit play roles critical to such Memory, these roles can potentially be differentiated and differences in the underlying synaptic and biochemical processes involved in each region are beginning to be uncovered.
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Interfering with Fos expression in rat perirhinal cortex impairs Recognition Memory.
Hippocampus, 2012Co-Authors: Ana Seoane, Chris J. Tinsley, Malcolm W. BrownAbstract:Previous work has shown that immunohistochemical imaging of Fos protein is a reliable marker for changes in activity related to Recognition Memory in the perirhinal cortex of the medial temporal lobe; however, whether perirhinal Fos expression is necessary for Recognition Memory had not been established. To investigate this potential requirement, antisense Fos oligodeoxynucleotide (ODN) was infused locally into perirhinal cortex to interfere with Fos production. As in previous studies, differential Fos expression produced by viewing novel or familiar visual stimuli was measured by immunohistochemistry: antisense Fos ODN infusion into perirhinal cortex disrupted the normal pattern of differential Fos expression in perirhinal cortex. The effect of antisense Fos ODN infusion into perirhinal cortex was therefore sought on Recognition Memory. Infusion before or immediately after acquisition impaired Recognition Memory for objects when the Memory delay was 3 h or 24 h, but not when the delay was 20 min, nor when the ODN was infused before retrieval after a 24 h delay. The findings indicate a role for Fos in consolidation processes underlying long-term Recognition Memory for objects and establish that interfering with its expression impairs Recognition Memory. Antisense Fos ODN infusion also impaired object-in-place Recognition Memory. The results demonstrate that Fos is necessary for neuronal mechanisms in perirhinal cortex essential to Recognition Memory.
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Contributions of area Te2 to rat Recognition Memory
Learning & memory (Cold Spring Harbor N.Y.), 2011Co-Authors: Katherine E Narduzzo, E C Warburton, Chris J. Tinsley, Alexandra Outram, Jeremy M. Henley, Malcolm W. BrownAbstract:Ablations and local intracerebral infusions were used to determine the role of rat temporal association cortex (area Te2) in object Recognition Memory, so that this role might be compared with that of the adjacent perirhinal cortex (PRH). Bilateral lesions of Te2 impaired Recognition Memory measured by preferential exploration of a novel rather than a familiar object at delays ≥20 min but not after a 5-min delay. Local infusion bilaterally into Te2 of (1) CNQX to block AMPA/kainate receptors or (2) lidocaine to block axonal transmission or (3) AP5, an NMDA receptor antagonist, impaired Recognition Memory after a 24-h but not a 20-min delay. In PRH all these manipulations impair Recognition Memory after a 20-min as well as a 24-h delay. UBP302, a GluK1 kainate receptor antagonist, impaired Recognition Memory after a 24-h but not a 20-min delay, contrasting with its action in PRH where it impairs only shorter-term (20 min) Recognition Memory. Also in contrast to PRH, infusion of the muscarinic receptor antagonist scopolamine was without effect. The Te2 impairments could not readily be ascribed to perceptual deficits. Hence, Te2 is essential for object Recognition Memory at delays >5 or 20 min. Thus, at long delays both area Te2 and PRH are necessary for object Recognition Memory.
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Recognition Memory: Material, processes, and substrates
Hippocampus, 2010Co-Authors: Malcolm W. Brown, E. Clea Warburton, John Patrick AggletonAbstract:The proposal that a system centering on the perirhinal cortex is responsible for familiarity discrimination, particularly for single items, whereas a system centering on the hippocampus is responsible for recollective and more complex associational aspects of Recognition Memory is reviewed in the light of recent findings. In particular, the proposal is reviewed in relation to recent animal work with rats and results from human clinical studies. Notably, progress has been made in determining potential neural Memory substrate mechanisms within the perirhinal cortex in rats. Recent findings have emphasized the importance of specifying the type of material, the type of test, and the strategy used by subjects to solve Recognition Memory tests if substrates are to be accurately inferred. It is to be expected that the default condition is that both the hippocampal and perirhinal systems will contribute to Recognition Memory performance. Indeed, rat lesion experiments provide examples of where cooperation between both systems is essential. Nevertheless, there remain examples of the independent operation of the hippocampal and perirhinal systems. Overall, it is concluded that most, though not all, of the recent findings are in support of the proposal. However, there is also evidence that the systems involved in Recognition Memory need to include structures outside the medial temporal lobe: there are significant but as yet only partially defined roles for the prefrontal cortex and sensory association cortices in Recognition Memory processes.
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Expression of Long-Term Depression Underlies Visual Recognition Memory
Neuron, 2008Co-Authors: Sarah Griffiths, Helen L. Scott, Alison S. Bienemann, Colin P J Glover, Malcolm W. Brown, Mohamed T Ghorbel, E. Clea Warburton, James B Uney, Zafar I. BashirAbstract:Summary The modifications occurring in the brain during learning and Memory are still poorly understood but may involve long-lasting changes in synaptic transmission (synaptic plasticity). In perirhinal cortex, a lasting decrement in neuronal responsiveness is associated with visual familiarity discrimination, leading to the hypothesis that long-term depression (LTD)-like synaptic plasticity may underlie Recognition Memory. LTD relies on internalization of AMPA receptors (AMPARs) through interaction between their GluR2 subunits and AP2, the clathrin adaptor protein required for endocytosis. We demonstrate that a peptide that blocks interactions between GluR2 and AP2 blocks LTD in perirhinal cortex in vitro. Viral transduction of this peptide in perirhinal cortex produced striking deficits in visual Recognition Memory. Furthermore, there was a deficit of LTD in perirhinal cortex slices from virally transduced, Recognition Memory-deficient animals. These results suggest that internalization of AMPA receptors, a process critical for the expression of LTD in perirhinal cortex, underlies visual Recognition Memory.
Federico Bermúdez-rattoni - One of the best experts on this subject based on the ideXlab platform.
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Molecular mechanisms of taste-Recognition Memory
Nature Reviews Neuroscience, 2004Co-Authors: Federico Bermúdez-rattoniAbstract:From an evolutionary point of view, one of the most important forms of Memory is taste-Recognition Memory. When an animal eats, food-related cues are associated with the consequences of its ingestion. So, if a new taste is associated with malaise, animals will reject it on the next presentation, developing a long-lasting taste aversion. Conversely, when taste is not accompanied by digestive malaise, it becomes recognized as a safe signal, and the animal increases its consumption. In this review, the putative molecular signals and biochemical events that mediate the formation of safe and aversive taste-Recognition Memory traces are discussed. Taste-Recognition Memory — the ability to identify a taste and relate it to past consequences of its ingestion — is extremely important from an evolutionary point of view. There are two forms of taste-Recognition Memory: safe and aversive taste Memory. They might be regulated by different neural pathways and seem to have different molecular mechanisms. The neuroanatomy of gustatory and visceral information is well established. There are different points of convergence in which the association between taste and its visceral consequences can be integrated. The best studied of these structures is the insular cortex. Safe taste Memory seems to involve cholinergic neurotransmission and its downstream signalling pathways, and its mechanisms might be related to those described for the processing of novelty in the nervous system. Aversive taste Memory also involves glutamatergic neurotransmission and its downstream signalling pathways, and other transmitters, such as the noradrenergic system, might have modulatory roles. For long-term taste Memory, protein synthesis is necessary. The extinction of aversive taste Memory seems to be independent of the cholinergic system, and its mechanisms seem to be related to those involved in the formation of aversive taste Memory.
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Molecular mechanisms of taste-Recognition Memory
Nature reviews. Neuroscience, 2004Co-Authors: Federico Bermúdez-rattoniAbstract:From an evolutionary point of view, one of the most important forms of Memory is taste-Recognition Memory. When an animal eats, food-related cues are associated with the consequences of its ingestion. So, if a new taste is associated with malaise, animals will reject it on the next presentation, developing a long-lasting taste aversion. Conversely, when taste is not accompanied by digestive malaise, it becomes recognized as a safe signal, and the animal increases its consumption. In this review, the putative molecular signals and biochemical events that mediate the formation of safe and aversive taste-Recognition Memory traces are discussed.
John Patrick Aggleton - One of the best experts on this subject based on the ideXlab platform.
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Recognition Memory: Material, processes, and substrates
Hippocampus, 2010Co-Authors: Malcolm W. Brown, E. Clea Warburton, John Patrick AggletonAbstract:The proposal that a system centering on the perirhinal cortex is responsible for familiarity discrimination, particularly for single items, whereas a system centering on the hippocampus is responsible for recollective and more complex associational aspects of Recognition Memory is reviewed in the light of recent findings. In particular, the proposal is reviewed in relation to recent animal work with rats and results from human clinical studies. Notably, progress has been made in determining potential neural Memory substrate mechanisms within the perirhinal cortex in rats. Recent findings have emphasized the importance of specifying the type of material, the type of test, and the strategy used by subjects to solve Recognition Memory tests if substrates are to be accurately inferred. It is to be expected that the default condition is that both the hippocampal and perirhinal systems will contribute to Recognition Memory performance. Indeed, rat lesion experiments provide examples of where cooperation between both systems is essential. Nevertheless, there remain examples of the independent operation of the hippocampal and perirhinal systems. Overall, it is concluded that most, though not all, of the recent findings are in support of the proposal. However, there is also evidence that the systems involved in Recognition Memory need to include structures outside the medial temporal lobe: there are significant but as yet only partially defined roles for the prefrontal cortex and sensory association cortices in Recognition Memory processes.
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interleaving brain systems for episodic and Recognition Memory
Trends in Cognitive Sciences, 2006Co-Authors: John Patrick Aggleton, Malcolm W. BrownAbstract:Conflicting models persist over the nature of long-term Memory. Crucial issues are whether episodic Memory and Recognition Memory reflect the same underlying processes, and the extent to which various brain structures work as a single unit to support these processes. New findings that have resulted from improved resolution of functional brain imaging, together with recent studies of amnesia and developments in animal testing, reinforce the view that Recognition Memory comprises at least two independent processes: one recollective and the other using familiarity detection. Only recollective Recognition appears to depend on episodic Memory. Attempts to map brain areas supporting these two putative components of Recognition Memory indicate that they depend on separate, but interlinked, structures.
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Benzodiazepine impairment of perirhinal cortical plasticity and Recognition Memory
The European journal of neuroscience, 2004Co-Authors: H Wan, Zafar I. Bashir, John Patrick Aggleton, E C Warburton, X. O. Zhu, Tim Koder, Y. Park, Kwangwook Cho, Malcolm W. BrownAbstract:Benzodiazepines, including lorazepam, are widely used in human medicine as anxiolytics or sedatives, and at higher doses can produce amnesia. Here we demonstrate that in rats lorazepam impairs both Recognition Memory and synaptic plastic processes (long-term depression and long-term potentiation). Both impairments are produced by actions in perirhinal cortex. The findings thus establish a mechanism by means of which benzodiazepines impair Recognition Memory. The findings also strengthen the hypotheses that the familiarity discrimination component of Recognition Memory is dependent on reductions in perirhinal neuronal responses when stimuli are repeated and that these response reductions are due to a plastic mechanism also used in long-term depression.
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Recognition Memory in rats-I. Concepts and classification
Progress in neurobiology, 1998Co-Authors: T. Steckler, W. H. I. M. Drinkenburg, A. Sahgal, John Patrick AggletonAbstract:Recognition is the process by which a subject is aware that a stimulus has been previously experienced. It requires that the characteristics of events are perceived, discriminated, identified and then compared (matched) against a Memory of the characteristics of previously experienced events. Understanding Recognition Memory, its underlying neuronal mechanisms, its dysfunction and alleviation of the latter by putative cognition enhancing drugs is a major research target and has triggered a wealth of animal studies. One of the most widely used animals for this purpose is the rat, and it is the rat's Recognition Memory which is the focus of this review. In this first part, concepts of Recognition Memory, stages of mnemonic processing and paradigms for the measurement of the rat's Recognition Memory will be discussed. In two subsequent articles (parts II and III) we will focus on the neuronal mechanisms underlying Recognition Memory in rats. Three major points arise from the comparison of paradigms that have in the past been used to assess Recognition Memory in rats. First, it should be realized that some tasks which, at face value, can all be considered to measure Recognition Memory in rats, may not assess Recognition Memory at all but may, for example, be based on recall rather than Recognition. Second, it is evident that different types of Recognition Memory can be distinguished and that tasks differ in the type of Recognition Memory taxed. Some paradigms, for example, measure familiarity, whereas others assess recency. Furthermore, paradigms differ as to whether spatial stimuli or items are employed. Third, different processes, ranging from stimulus–response learning to the formation of concepts, may be involved to varying extent in different tasks. These are important considerations and question the predictive validity of the results obtained from studies examining, for example, the effects of putative cognition enhancing drugs.
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Recognition Memory in rats—III. Neurochemical substrates
Progress in neurobiology, 1998Co-Authors: T. Steckler, John Patrick Aggleton, A. Sahgal, W. H. I. M. DrinkenburgAbstract:In the first part of three overviews on Recognition Memory in the rat, we discussed the tasks employed to study Recognition Memory. In the second part, we discussed the neuroanatomical systems thought to be of importance for the mediation of Recognition Memory in the rat. In particular, we delineated two parallel-distributed neuronal networks, one that is essential for the processing of non-spatial/item Recognition Memory processes and incorporates the cortical association areas such as TE1, TE2 and TE3, the rhinal cortices, the mediodorsal thalamic nucleus and prefrontal cortical areas (Network 1), the other comprising of the hippocampus, mamillary bodies, anterior thalamic nuclei and medial prefrontal areas (Network 2), suggested to be pivotal for the processing of spatial Recognition Memory. The next step will progress to the level of the neurotransmitters thought to be involved. Current data suggest that the majority of drugs have non-specific, i.e. delay-independent effects in tasks measuring Recognition Memory. This may be due to attentional, motivational or motoric changes. Alternatively, delay-independent effects may result from altered acquisition/encoding rather than from altered retention. Furthermore, the neurotransmitter systems affected by these drugs could be important as modulators rather than as mediators of Recognition Memory per se. It could, of course, also be the case that systemic treatment induces non-specific effects which overshadow any specific, delay-dependent, effect. This possibility receives support from lesion experiments (for example, of the septohippocampal cholinergic system) or studies employing local intracerebral infusion techniques. However, it is evident that those delay-dependent effects are relatively subtle and more readily seen in delayed response paradigms, which tax spatial Recognition Memory. One interpretation of these results could be that some neurotransmitter systems are more involved in spatial than in item Recognition Memory processes. However, performance in delayed response tasks can be aided by mediating strategies. Drugs or lesions can alter those strategies, which could equally explain some of the (delay-dependent) drug effects on delayed responding. Thus, it is evident that neither of the neurotransmitter systems reviewed (glutamate, GABA, acetylcholine, serotonin, dopamine and noradrenaline) can be viewed as being directly and exclusively concerned with storage/retention. Rather, our model of Recognition Memory suggests that information about previously encountered items is differentially processed by distinct neural networks and is not mediated by a single neurotransmitter type.
E C Warburton - One of the best experts on this subject based on the ideXlab platform.
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Using the Spontaneous Object Recognition Memory Tasks to Uncover the Neural Circuitry of Recognition Memory: The Importance of Thalamic Nuclei
Handbook of Object Novelty Recognition, 2018Co-Authors: E C WarburtonAbstract:Abstract Recognition Memory, our ability to distinguish between novel and familiar objects or places, is central to our ability to recall day-to-day events or plan future behaviours. Recognition Memory judgements can be made using different types of information, and the type of information utilized determines the involvement of distinct brain structures. Studies have explored the neural basis of Recognition Memory through an examination of the effects of specific lesions in defined brain regions on Recognition Memory using the novel object preference task and its variants. These studies have implicated a neural circuit involving the perirhinal cortex, hippocampus and medial prefrontal cortex in object-in-place Memory and temporal order Memory. Recognition of single items, in contrast, appears to rely on the perirhinal cortex. Here I present evidence that in addition to these cortical and subcortical regions, the role of three thalamic regions, the medial dorsal thalamus, anterior thalamic nuclei and the midline thalamus must also now be considered.
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Neural circuitry for rat Recognition Memory
Behavioural brain research, 2014Co-Authors: E C Warburton, Malcolm W. BrownAbstract:Information concerning the roles of different brain regions in Recognition Memory processes is reviewed. The review concentrates on findings from spontaneous Recognition Memory tasks performed by rats, including Memory for single objects, locations, object–location associations and temporal order. Particular emphasis is given to the potential roles of different regions in the circuit of interacting structures involving the perirhinal cortex, hippocampus, medial prefrontal cortex and medial dorsal thalamus in Recognition Memory for the association of objects and places. It is concluded that while all structures in this circuit play roles critical to such Memory, these roles can potentially be differentiated and differences in the underlying synaptic and biochemical processes involved in each region are beginning to be uncovered.
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when is the hippocampus involved in Recognition Memory
The Journal of Neuroscience, 2011Co-Authors: Gareth R I Barker, E C WarburtonAbstract:The role of the hippocampus in Recognition Memory is controversial. Recognition Memory judgments may be made using different types of information, including object familiarity, an object9s spatial location, or when an object was encountered. Experiment 1 examined the role of the hippocampus in Recognition Memory tasks that required the animals to use these different types of mnemonic information. Rats with bilateral cytotoxic lesions in the hippocampus or perirhinal or prefrontal cortex were tested on a battery of spontaneous object Recognition tasks requiring the animals to make Recognition Memory judgments using familiarity (novel object preference); object–place information (object-in-place Memory), or recency information (temporal order Memory). Experiment 2 examined whether, when using different types of Recognition Memory information, the hippocampus interacts with either the perirhinal or prefrontal cortex. Thus, groups of rats were prepared with a unilateral cytotoxic lesion in the hippocampus combined with a lesion in either the contralateral perirhinal or prefrontal cortex. Rats were then tested in a series of object Recognition Memory tasks. Experiment 1 revealed that the hippocampus was crucial for object location, object-in-place, and recency Recognition Memory, but not for the novel object preference task. Experiment 2 revealed that object-in-place and recency Recognition Memory performance depended on a functional interaction between the hippocampus and either the perirhinal or medial prefrontal cortices. Thus, the hippocampus plays a role in Recognition Memory when such Memory involves remembering that a particular stimulus occurred in a particular place or when the Memory contains a temporal or object recency component.
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Contributions of area Te2 to rat Recognition Memory
Learning & memory (Cold Spring Harbor N.Y.), 2011Co-Authors: Katherine E Narduzzo, E C Warburton, Chris J. Tinsley, Alexandra Outram, Jeremy M. Henley, Malcolm W. BrownAbstract:Ablations and local intracerebral infusions were used to determine the role of rat temporal association cortex (area Te2) in object Recognition Memory, so that this role might be compared with that of the adjacent perirhinal cortex (PRH). Bilateral lesions of Te2 impaired Recognition Memory measured by preferential exploration of a novel rather than a familiar object at delays ≥20 min but not after a 5-min delay. Local infusion bilaterally into Te2 of (1) CNQX to block AMPA/kainate receptors or (2) lidocaine to block axonal transmission or (3) AP5, an NMDA receptor antagonist, impaired Recognition Memory after a 24-h but not a 20-min delay. In PRH all these manipulations impair Recognition Memory after a 20-min as well as a 24-h delay. UBP302, a GluK1 kainate receptor antagonist, impaired Recognition Memory after a 24-h but not a 20-min delay, contrasting with its action in PRH where it impairs only shorter-term (20 min) Recognition Memory. Also in contrast to PRH, infusion of the muscarinic receptor antagonist scopolamine was without effect. The Te2 impairments could not readily be ascribed to perceptual deficits. Hence, Te2 is essential for object Recognition Memory at delays >5 or 20 min. Thus, at long delays both area Te2 and PRH are necessary for object Recognition Memory.
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Benzodiazepine impairment of perirhinal cortical plasticity and Recognition Memory
The European journal of neuroscience, 2004Co-Authors: H Wan, Zafar I. Bashir, John Patrick Aggleton, E C Warburton, X. O. Zhu, Tim Koder, Y. Park, Kwangwook Cho, Malcolm W. BrownAbstract:Benzodiazepines, including lorazepam, are widely used in human medicine as anxiolytics or sedatives, and at higher doses can produce amnesia. Here we demonstrate that in rats lorazepam impairs both Recognition Memory and synaptic plastic processes (long-term depression and long-term potentiation). Both impairments are produced by actions in perirhinal cortex. The findings thus establish a mechanism by means of which benzodiazepines impair Recognition Memory. The findings also strengthen the hypotheses that the familiarity discrimination component of Recognition Memory is dependent on reductions in perirhinal neuronal responses when stimuli are repeated and that these response reductions are due to a plastic mechanism also used in long-term depression.
