Effects of thalamic and olfactory cortical lesions on continuous olfactory delayed nonmatching-to-sample and olfactory discrimination in rats (Rattus norvegicus).

Zhang, Yueping; Burk, Joshua A.; Glode, Barbara M.; Mair, Robert G.

doi:10.1037/0735-7044.112.1.39

Cited by 43 publications

(66 citation statements)

References 25 publications

(62 reference statements)

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“…It is also possible that the lack of any further deficit in the LT group with the extension of the intratrial delay to 20 sec was due to some degree of recovery of function, although no obvious recovery was apparent in the 10 sessions immediately prior to testing the longer delay. There is, however, other evidence that delay-independent deficits may be a consistent feature across a variety of tasks after both large (Young et al 1996;Burk and Mair 1998;Zhang et al 1998) and, now, selective lesions centered on the ILn region (the current findings; Bailey and Mair 2005). Such Table 1 for inclusion/exclusion details.…”

Section: Discussionmentioning

confidence: 62%

“…In contrast, a broader range of deficits is associated with ILn lesions and, coupled with the suggestion that only modest or more selective effects occur after localized AT lesions, this evidence has provided the impetus to suggest that ILn damage is a more essential source of thalamic amnesia (Mair et al 2003). For example, there are several reports that large ILn lesions produce delay-independent deficits in both spatial and olfactory tasks and evidence that this thalamic region is involved in egocentric response-related processing (Harrison and Mair 1996;Young et al 1996;Burk and Mair 1998;Mair et al 1998;Zhang et al 1998).…”

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confidence: 99%

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Lateral and anterior thalamic lesions impair independent memory systems

Mitchell¹,

Dalrymple‐Alford²

2006

Learn. Mem.

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Damage to the medial region of the thalamus, both in clinical cases (e.g., patients with infarcts or the Korsakoff's syndrome) and animal lesion models, is associated with variable amnesic deficits. Some studies suggest that many of these memory deficits rely on the presence of lateral thalamic lesions (LT) that include the intralaminar nuclei, presumably by altering normal function between the striatum and frontal cortex. Other studies suggest that the anterior thalamic nuclei (AT) may be more critical, as a result of disruption to an extended hippocampal system. Here, highly selective LT and AT lesions were made to test the prediction that these two regions contribute to two different memory systems. Only LT lesions produced deficits on a preoperatively acquired response-related (egocentric) working memory task, tested in a cross-maze. Conversely, only AT lesions impaired postoperative acquisition of spatial working memory, tested in a radial maze. These findings provide the first direct evidence of a double dissociation between the LT and AT neural aggregates. As the lateral and the anterior medial thalamus influence parallel independent memory processing systems, they may each contribute to memory deficits, depending on lesion extent in clinical and experimental cases of thalamic amnesia.Profound memory deficits including disruptions to allocentric (place-related) and egocentric (response-related) spatial information processing may occur following medial thalamic injury in humans (Holdstock et al. 1999;Kopelman 2002;Van der Werf et al. 2000, 2003. The source of these impairments is uncertain, with recent reports emphasizing either the intralaminar (ILn) or the anterior (AT) thalamic nuclei (Graff-Radford et al. 1990;Aggleton and Brown 1999;Harding et al. 2000;Mair et al. 2003). Damage to the AT in animal models mimics many of the allocentric spatial memory deficits associated with hippocampal system damage, which is believed to be a key indicator of episodic memory loss (

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Section: Discussionmentioning

confidence: 62%

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confidence: 99%

Lateral and anterior thalamic lesions impair independent memory systems

Mitchell¹,

Dalrymple‐Alford²

2006

Learn. Mem.

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“…From the olfactory cortex, there is a substantial projection to the mediodorsal thalamus and the ventral part of the submedius nucleus (SM), which in turn projects to the frontal cortex [40]. Disruption of these connections results in deficits in complex but not in simple odour discrimination tasks [41][42][43]. Another small projection from the LOT goes to the lateral entorhinal cortex [44] and thence via the perforant path to the dentate gyrus and CA1/CA3 of the hippocampus.…”

Section: The Main Olfactory System (Mos)mentioning

confidence: 99%

Neural Encoding of Olfactory Recognition Memory

Sánchez-Andrade

James

Kendrick

2005

Journal of Reproduction and Development

102

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Abstract. Our work with both sheep and mouse models has revealed many of the neural substrates and signalling pathways involved in olfactory recognition memory in the main olfactory system. A distributed neural system is required for initial memory formation and its short-term retention-the olfactory bulb, piriform and entorhinal cortices and hippocampus. Following memory consolidation, after 8 h or so, only the olfactory bulb and piriform cortex appear to be important for effective recall. Similarly, whereas the glutamate-NMDA/AMPA receptor-nitric oxide (NO)-cyclic GMP signalling pathway is important for memory formation it is not involved in recall post-consolidation. Here, within the olfactory bulb, up-regulation of class 1 metabotropic glutamate receptors appears to maintain the enhanced sensitivity at the mitral to granule cell synapses required for effective memory recall. Recently we have investigated whether fluctuating sex hormone levels during the oestrous cycle modulate olfactory recognition memory and the different neural substrates and signalling pathways involved. These studies have used two robust models of social olfactory memory in the mouse which either involve social or non social odours (habituation-dishabituation and social transmission of food preference tasks). In both cases significant improvement of learning retention occurs when original learning takes place during the proestrus phase of the ovarian cycle. This is probably the result of oestrogen changes at this time since transgenic mice lacking functional expression of oestrogen receptors (ERα and ERβ, the two main oestrogen receptor sub-types) have shown problems in social recognition. Therefore, oestrogen appears to act at the level of the olfactory bulb by modulating both noradrenaline and the glutamate/NO signalling pathway. Key words: Olfactory bulb, Olfactory memory, Olfactory recognition, Social learning, Nitric oxide (NO), Oestrous cycle, Sheep, Mouse, Social transmission of food preference (J. Reprod. Dev. 51: [547][548][549][550][551][552][553][554][555][556][557][558] 2005) or several decades, olfactory learning has been used as a model for the study of memory. This is not only because mammalian olfactory learning shows a number of features common to the human declarative memory system one-trial learning, rapid encoding, long lasting memories and a high capacity for information storage-but also because olfactory memory models represent a relatively simple form of learning and the olfactory system has well characterised pathways and structural organisation which offers many advantages in defining how processing occurs at a systems level. This makes it feasible to study plasticity at all levels in the system, from the initial sensory detection of odourant molecules at the level of the olfactory receptors righ t thr ough to high er cortical processing.There are many different forms of olfactory learning and memory in diverse behavioural contexts involving different mechanisms within the olfactory system. Olfactory learning ...

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“…While some of the cognitive impairments associated with WKS have been found to respond positively to treatment with catecholaminergic or serotonergic drugs, none of these treatments has resulted in clinically significant improvements in mnemonic function (Mair and McEntee 1986;McEntee and Mair 1990;McEntee and Crook 1991). Recent studies of animal models of WKS have identified the intralaminar thalamic nuclei (ILn) as a critical site of pathology, that is: (i) sensitive to the effects of thiamin deficiency, the main etiologic factor in WKS; (ii) consistent with the location of lesions observed in WKS; and (iii) a location where lesions in animal models disrupt performance of delayed conditional discrimination tasks used to measure remembering in multiple sensory modalities Mair et al 1998;Zhang et al 1998; see Mair 1994 for review).…”

Section: Introductionmentioning

confidence: 96%

“…Lesions affecting the ILn have been found to increase the latency and to decrease the accuracy of responding in a delay-independent fashion for delayed non-matching (DNMS) and matching (DMS) to sample tasks, whether these lesions are produced by thiamin deficiency (Knoth and Mair 1991;Robinson and Mair 1992), electrolytic heating (Mair and Lacourse 1992;Koger and Mair 1994;Young et al 1996), or excitotoxic treatment Mair et al 1998;Zhang et al 1998). BDZ agonists also have been reported to impair both the speed and the accuracy of responding on delayed conditional discrimination tasks used to measure working memory, although these tasks differ from the procedures that have been used to measure the effects of ILn lesions on remembering (McNaughton and Morris 1987;Tan et al 1990;Ohno et al 1992;Cole and Hillman 1994).…”

Section: Introductionmentioning

confidence: 98%

Effects of chlordiazepoxide and FG 7142 on a rat model of diencephalic amnesia as measured by delayed-matching-to-sample performance

et al. 1999

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The intralaminar thalamic nuclei (ILn) have been implicated as a critical site of pathology in amnesia. Lesions of the ILn have been found to produce behavioral effects comparable to benzodiazepine (BDZ) receptor agonists. We compared the effects of chlordiazepoxide (CDP), a BDZ agonist, and FG 7142, a partial inverse agonist at the BDZ receptor, in rats with thalamic lesions and in unlesioned controls. Delayed matching-to sample (DMS) performances were studied during treatment with ascending doses of CDP, counterbalanced trials with 2.5 mg/kg CDP and saline, ascending doses of FG 7142, and (for unlesioned controls only) counterbalanced trials with saline and higher doses of CDP. CDP had effects similar to the ILn lesion, decreasing response speed and percent correct responding in a delay-independent fashion. These effects were additive with the impairments associated with the ILn lesion. The effects of FG 7142 were more complex. At lower doses, it increased response speed without affecting response accuracy. At higher doses, it diminished both the speed and the accuracy of DMS responding. These results support the hypothesis that ILn lesions and BDZ agonists have similar effects on DMS performance. The biphasic effects observed for FG 7142 are consistent with other evidence that low doses of this drug enhance while higher doses impair memory performance. Although DMS accuracy was not improved, the enhancement observed for response speed provides evidence that partial inverse BDZ agonists have potential utility as treatments for cognitive impairments associated with amnesia.

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Effects of thalamic and olfactory cortical lesions on continuous olfactory delayed nonmatching-to-sample and olfactory discrimination in rats (Rattus norvegicus).

Cited by 43 publications

References 25 publications

Lateral and anterior thalamic lesions impair independent memory systems

Lateral and anterior thalamic lesions impair independent memory systems

Neural Encoding of Olfactory Recognition Memory

Effects of chlordiazepoxide and FG 7142 on a rat model of diencephalic amnesia as measured by delayed-matching-to-sample performance

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