Spatial memory, recognition memory, and the hippocampus

Broadbent, Nicola; Squire, Larry R.; Clark, Robert E.

doi:10.1073/pnas.0406344101

Cited by 825 publications

(635 citation statements)

References 39 publications

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“…It has been suggested that spatial memory requires a more complete hippocampal function than does recognition memory (Broadbent et al, 2004) so it seems that the 4-week treatment was enough to improve the function in different brain areas related to recognition memory but not in the hippocampus. A longer-lasting rosiglitazone treatment also rescued impaired spatial memory.…”

Section: Discussionmentioning

confidence: 99%

Rosiglitazone Rescues Memory Impairment in Alzheimer's Transgenic Mice: Mechanisms Involving a Reduced Amyloid and Tau Pathology

Escribano

Simón

Gimeno

et al. 2010

Neuropsychopharmacol

199

139

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Clinical studies suggest that agonists at peroxisome proliferator-activated receptor gamma (PPARg) may exert beneficial effects in patients with mild-to-moderate Alzheimer's disease (AD), but the mechanism for the potential therapeutic interest of this class of drugs has not yet been elucidated. Here, in mice overexpressing mutant human amyloid precursor protein, we found that chronic treatment with rosiglitazone, a high-affinity agonist at PPARg, facilitated b-amyloid peptide (Ab) clearance. Rosiglitazone not only reduced Ab burden in the brain but, importantly, almost completely removed the abundant amyloid plaques observed in the hippocampus and entorhinal cortex of 13-month-old transgenic mice. In the hippocampus, neuropil threads containing phosphorylated tau, probably corresponding to dystrophic neurites, were also decreased by the drug. Rosiglitazone switched on the activated microglial phenotype, promoting its phagocytic ability, reducing the expression of proinflammatory markers and inducing factors for alternative differentiation. The decreased amyloid pathology may account for the reduction of p-tau-containing neuropil threads and for the rescue of impaired recognition and spatial memory in the transgenic mice. This study provides further insights into the mechanisms for the beneficial effect of rosiglitazone in AD patients.

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Section: Discussionmentioning

confidence: 99%

Rosiglitazone Rescues Memory Impairment in Alzheimer's Transgenic Mice: Mechanisms Involving a Reduced Amyloid and Tau Pathology

Escribano

Simón

Gimeno

et al. 2010

Neuropsychopharmacol

199

139

View full text Add to dashboard Cite

show abstract

“…In studies that examine recognition by monitoring spontaneous exploration of familiar and novel stimuli, monkeys with selective hippocampal or parahippocampal cortex damage that show little or no deficit in DNMS have severe and rapidly apparent deficits on the spontaneous novelty exploration task Nemanic et al, 2004). In rats, some studies report no deficit (e.g., Mumby, 2001;Mumby et al, 2002;Winters et al, 2004), whereas other studies have observed impairment at long delays Hammond et al, 2004), or following a large amount of damage to the hippocampus (Broadbent et al, 2004). In contrast to the modest and variable deficit observed following damage to the hippocampus, ablation of the perirhinal cortex consistently results in a severe and rapidly developing deficit in both kinds of recognition memory tasks in monkeys (Nemanic et al, 2004) and in rats (Mumby et al, 2002;Winters et al, 2004;Norman and Eacott, 2005;Winters and Bussey, 2005).…”

Section: Hippocampusmentioning

confidence: 98%

Towards a functional organization of the medial temporal lobe memory system: Role of the parahippocampal and medial entorhinal cortical areas

2008

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ABSTRACT:Whereas substantial recent evidence has suggested to some that the medial entorhinal cortex (MEC) plays a specialized role in spatial navigation, here we present evidence consistent with a broader role of the MEC in memory. A consideration of evidence on the anatomy and functional roles of medial temporal cortical areas and the hippocampus, and evidence from recordings from MEC neurons in rats performing a spatial memory task, suggest that the MEC may process information about both spatial and temporal context in support of episodic memory. V

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“…Hippocampal damage from ibotenic acid disrupted recognition memory in the novel object recognition task and the visual paired comparison task (Clark et al, 2000;Broadbent et al, 2004). Furthermore, an intrahippocampal WIN 55,212-2, also impaired performance of the novel object recognition task (Kosiorek et al, 2003;Suenaga and Ichitani, 2008).…”

Section: Discussionmentioning

confidence: 99%

A Cannabinoid CB1 Receptor Antagonist Ameliorates Impairment of Recognition Memory on Withdrawal from MDMA (Ecstasy)

Nawata

Hiranita

Yamamoto

2009

Neuropsychopharmacol

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( + /À)-3,4-Methylenedioxymethamphetamine (MDMA, 'Ecstasy') abusers have persistent neuropsychiatric deficits including memory impairments after the cessation of abuse. On the other hand, cannabinoid CB 1 receptors have been implicated in learning/memory, and are highly expressed in the hippocampus, a region of the brain believed to have an important function in certain forms of learning and memory. In this study, we clarified the mechanism underlying the cognitive impairment that develops during MDMA withdrawal from the standpoint of the cannabinoid CB 1 receptors. Mice were administered MDMA (10 mg/kg, i.p.) once a day for 7 days. On the 7th day of withdrawal, a novel object recognition task was performed and the amount of cannabinoid CB 1 receptor protein was measured with western blotting. Recognition performance was impaired on the 7th day of withdrawal. This impairment was blocked by AM251, a cannabinoid CB 1 receptor antagonist, administered 30 min before the training trial or co-administered with MDMA. At this time, the level of cannabinoid CB 1 receptor protein increased significantly in the hippocampus but not the prefrontal cortex or striatum. This increase of CB 1 receptor protein in the hippocampus was also blocked by the co-administration of AM251. Furthermore, CB 1 receptor knockout mice showed no impairment of recognition performance on the withdrawal from MDMA. The impairment of recognition memory during withdrawal from MDMA may result from the activation of cannabinoid CB 1 receptors in the hippocampus.

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Spatial memory, recognition memory, and the hippocampus

Cited by 825 publications

References 39 publications

Rosiglitazone Rescues Memory Impairment in Alzheimer's Transgenic Mice: Mechanisms Involving a Reduced Amyloid and Tau Pathology

Rosiglitazone Rescues Memory Impairment in Alzheimer's Transgenic Mice: Mechanisms Involving a Reduced Amyloid and Tau Pathology

Towards a functional organization of the medial temporal lobe memory system: Role of the parahippocampal and medial entorhinal cortical areas

A Cannabinoid CB1 Receptor Antagonist Ameliorates Impairment of Recognition Memory on Withdrawal from MDMA (Ecstasy)

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