Associative recognition and the hippocampus: Differential effects of hippocampal lesions on object‐place, object‐context and object‐place‐context memory

Langston, Rosamund F.; Wood, Emma R.

doi:10.1002/hipo.20714

Cited by 209 publications

(221 citation statements)

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“…Previous studies have demonstrated that recognition memory can be impaired by lesions on the PFC in monkeys and rats (Bachevalier andMishkin, 1986, Kolb et al , 1994). On the other hand, studies in rodents showed contradictory results regarding the implication the hippocampus in recognition memory, reporting that hippocampal lesions may have no effect in object recognition memory in rats (Forwood et al , 2005, Langston and Wood, 2010, Mumby et al , 2002. This suggests that the PFC may have a more influential role in recognition memory compared to the hippocampus in rodents.…”

Section: Bardoxolone Methyl Prevented Hf Diet Induced Decline In Downmentioning

confidence: 99%

Bardoxolone methyl prevents high-fat diet-induced alterations in prefrontal cortex signalling molecules involved in recognition memory

Camer

Szabo

et al. 2015

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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X. (2015). Bardoxolone methyl prevents high-fat diet-induced alterations in prefrontal cortex signalling molecules involved in recognition memory. Progress in Neuro-Psychopharmacology and Biological Psychiatry, 59 68-75. Bardoxolone methyl prevents high-fat diet-induced alterations in prefrontal cortex signalling molecules involved in recognition memory AbstractHigh fat (HF) diets are known to induce changes in synaptic plasticity in the forebrain leading to learning and memory impairments. Previous studies of oleanolic acid derivatives have found that these compounds can cross the blood-brain barrier to prevent neuronal cell death. We examined the hypothesis that the oleanolic acid derivative, bardoxolone methyl (BM) would prevent diet-induced cognitive deficits in mice fed a HF diet. C57BL/6J male mice were fed a lab chow (LC) (5% of energy as fat), a HF (40% of energy as fat), or a HF diet supplemented with 10 mg/kg/day BM orally for 21 weeks. Recognition memory was assessed by performing a novel object recognition test on the treated mice. Downstream brain-derived neurotrophic factor (BDNF) signalling molecules were examined in the prefrontal cortex (PFC) and hippocampus of mice via Western blotting and N-methyl-d-aspartate (NMDA) receptor binding. BM treatment prevented HF dietinduced impairment in recognition memory (p < 0.001). In HF diet fed mice, BM administration attenuated alterations in the NMDA receptor binding density in the PFC (p < 0.05), however, no changes were seen in the hippocampus (p > 0.05). In the PFC and hippocampus of the HF diet fed mice, BM administration improved downstream BDNF signalling as indicated by increased protein levels of BDNF, phosphorylated tropomyosin related kinase B (pTrkB) and phosphorylated protein kinase B (pAkt), and increased phosphorylated AMP-activated protein kinase (pAMPK) (p < 0.05). BM administration also prevented the HF diet-induced increase in the protein levels of inflammatory molecules, phosphorylated c-Jun N-terminal kinase (pJNK) in the PFC, and protein tyrosine phosphatase 1B (PTP1B) in both the PFC and hippocampus. In summary, these findings suggest that BM prevents HF diet-induced impairments in recognition memory by improving downstream BDNF signal transduction, increasing pAMPK, and reducing inflammation in the PFC and hippocampus. AbstractHigh-fat (HF) diets are known to induce changes in synaptic plasticity in the forebrain leading to learning and memory impairments. Previous studies of oleanolic acid derivatives have found that these compounds can cross the blood brain barrier to prevent neuronal cell death. We examined the hypothesis that the oleanolic acid derivative, bardoxolone methyl (BM) would prevent diet-induced cognitive deficits in mice fed a HF diet. C57BL/6J male mice were fed a lab chow (LC) (5% of energy as fat), HF (40% of energy as fat), or HF diet supplemented with 10 mg/kg/day BM orally for 21 weeks. and phosphorylated protein kinase B (pAkt), and increased phosphorylated AMP-activated protein kinase (pAMPK) (p<0.05). BM a...

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Section: Bardoxolone Methyl Prevented Hf Diet Induced Decline In Downmentioning

confidence: 99%

Bardoxolone methyl prevents high-fat diet-induced alterations in prefrontal cortex signalling molecules involved in recognition memory

Camer

Szabo

et al. 2015

Progress in Neuro-Psychopharmacology and Biological Psychiatry

View full text Add to dashboard Cite

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“…We defined exploration as sniffing or touching the stimuli objects with the muzzle and/or forepaws. A discrimination index (DI = (Time exploring novel object À Time exploring familiar object)/Total object exploration time) was used as a measure of discrimination between familiar and novel objects (Aggleton, Albasser, Aggleton, Poirier, & Pearce, 2010;Aubele, Kaufman, Montalmant, & Kritzer, 2008;Langston & Wood, 2010;Cohen et al, 2008;Till et al, 2015). DI varies between À1 and +1.…”

Section: Behavioral Procedures and Data Analysismentioning

confidence: 99%

BDNF controls object recognition memory reconsolidation

Radiske

Rossato

Gonzalez

et al. 2017

Neurobiology of Learning and Memory

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a-amanitinMuscimol Novelty Retrieval a b s t r a c t Reconsolidation restabilizes memory after reactivation. Previously, we reported that the hippocampus is engaged in object recognition memory reconsolidation to allow incorporation of new information into the original engram. Here we show that BDNF is sufficient for this process, and that blockade of BDNF function in dorsal CA 1 impairs updating of the reactivated recognition memory trace.

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“…While a number of studies show that hippocampal or fornix lesions produce no effect in object recognition (Bussey et al, 2000;Mumby et al, 2002;Winters et al, 2004;Forwood et al, 2005;Good et al, 2007;Langston and Wood, 2010), other studies report significant impairments (Clark et al, 2000(Clark et al, , 2001). In contrast, object-in-place memory is impaired following fornix lesions (Bussey et al, 2000) and hippocampal lesions impair temporal order discriminations (Kesner and Novak, 1982;Chiba et al, 1994;Vorobyov, 1998;Fortin et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

When Is the Hippocampus Involved in Recognition Memory?

Barker¹,

Warburton²

2011

Journal of Neuroscience

697

634

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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 object's 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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Associative recognition and the hippocampus: Differential effects of hippocampal lesions on object‐place, object‐context and object‐place‐context memory

Cited by 209 publications

References 54 publications

Bardoxolone methyl prevents high-fat diet-induced alterations in prefrontal cortex signalling molecules involved in recognition memory

Bardoxolone methyl prevents high-fat diet-induced alterations in prefrontal cortex signalling molecules involved in recognition memory

BDNF controls object recognition memory reconsolidation

When Is the Hippocampus Involved in Recognition Memory?

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