Hippocampal degeneration inducing impairment of learning in rats: model of dementia?

Ito, Koichi; Kubo, Toshio; Shibanoki, Shinji; Matsumoto, Akira; Hata, Hideyo; Asai, Satoshi

doi:10.1016/s0166-4328(97)86043-3

Cited by 55 publications

(34 citation statements)

References 22 publications

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“…CA1 of hippocampus, which develops dense accumulations of neuro®brillary tangles in Alzheimer's disease, is an area of the brain that appears to be involved in many types of memory (Rotenberg et al, 1996;Ishikawa et al, 1997;Ridley and Baker, 1997). In our memory experiments with rodents, MAP-2 degradation related to contextual memory occurred in CA1 of hippocampus 2 weeks after training.…”

Section: Memory Storage and Agingmentioning

confidence: 60%

A structural basis for memory storage in mammals

Woolf

1998

Progress in Neurobiology

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AbstractÐIt is proposed that altered dendrite length and de novo formation of new dendrite branches in cholinoceptive cells are responsible for long-term memory storage, a process enabled by the degradation of microtubule-associated protein-2. These memories are encoded as modality-speci®c associable representations. Accordingly, associable representations are con®ned to cytoarchitectonic modules of the cerebral cortex, hippocampus, and amygdala. The proposed sequence of events leading to long-term storage in cholinoceptive dendrites begins with changes in neuronal activity, then in neurotrophin release, followed by enhanced acetylcholine release, muscarinic response, calcium in¯ux, degradation of microtubule-associated protein-2, and ®nally new dendrite structure. Hypothetically, each associable representation consists of altered dendrite segments from approximately 5000±15 000 cholinoceptive cells contained within one or a few module(s). Simultaneous restructuring during consolidation of long-term memory is hypothesized to result in a similar infrastructure among dendrite sets, facilitating co-activation of those dendrite sets by neurotransmitters such as acetylcholine, and conceivably enabling high energy interactions between those dendrites by phenomena such as quantum optical coherence. Based on the speci®c architecture proposed, it is estimated that the human telencephalon contains enough dendrites to encode 50 million associable representations in a lifetime, or put another way, to encode one new associable representation each minute. The implications that this proposal has regarding treatments for Alzheimer's disease are also discussed. #

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Section: Memory Storage and Agingmentioning

confidence: 60%

A structural basis for memory storage in mammals

Woolf

1998

Progress in Neurobiology

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“…It has been reported that MSG has some adverse effects in humans (Plaitakis & Shashidharan, 2000;Piližota, 2010). The administration of high doses of MSG during early stages of brain development, when animals have an immature blood-brain barrier, induces destruction of sites in the hypothalamus and selective degeneration in hippocampal CA1 pyramidal cells (Abe et al 1990;Ishikawa et al 1997). In general, the induction of glutamate neurotoxicity involves the development of intracellular changes and subsequent events resulting in neuronal disintegration (Choi, 1994).…”

Section: Introductionmentioning

confidence: 99%

Resistance exercise reduces memory impairment induced by monosodium glutamate in male and female rats

Araujo

Quines

Jardim

et al. 2017

Experimental Physiology

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Edited by: Michael White New Findings r What is the central question of this study?Monosodium glutamate causes cognitive impairment. Does resistance exercise improve the performance of rats treated with monosodium glutamate? r What is the main finding and its importance?Resistance exercise is effective against monosodium glutamate-induced memory impairment in male and female rats.Monosodium glutamate (MSG), a flavour enhancer in diets, causes cognitive impairment in rodents. Exercise has been reported to protect against impairment of memory in humans. In this study, we investigated whether resistance exercise improves the performance of male and female rats treated with MSG in tests of memory and motor co-ordination. Wistar rats received MSG [4 g (kg body weight) −1 day −1 , s.c.] from postnatal day 1 to 10. At postnatal day 60, the animals started a resistance exercise protocol in an 80 deg inclined vertical ladder apparatus and performed it during 7 weeks. Rats performed object recognition and location memory tests. Resistance exercise reduced impairment in motor co-ordination of male and female rats treated with MSG. Resistance exercise was effective against the decrease in exploratory preference in the long-term recognition memory for novel objects of male rats treated with MSG. In MSG-treated female rats, resistance exercise was effective against the decrease in exploratory preference in the novel object location test. The exploratory preference of female rats in the long-term recognition memory test was similar in all groups. The short-term memory was not altered by MSG or resistance exercise in male and female rats. This study demonstrates that MSG affected the memory of male and female rats in different ways. Resistance exercise was effective against the decrease in recognition for male rats and in location memory for female rats treated with MSG. This report demonstrates the beneficial effects of resistance exercise against the prejudice of motor condition and impairment of memory induced by MSG in male and female rats.

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“…In this study, we used an in vitro model of Glu-induced excitotoxicity in SH-SY5Y cells and an in vivo dementia model of perinatal monosodium glutamate (MSG) exposure [18] to investigate the neuroprotective functions of AA and its possible mechanisms of action.…”

Section: Introductionmentioning

confidence: 99%

Asiatic acid, a pentacyclic triterpene in Centella asiatica, attenuates glutamate-induced cognitive deficits in mice and apoptosis in SH-SY5Y cells

et al. 2012

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Aim: To investigate whether asiatic acid (AA), a pentacyclic triterpene in Centella asiatica, exerted neuroprotective effects in vitro and in vivo, and to determine the underlying mechanisms. Methods: human neuroblastoma Sh-SY5Y cells were used for in vitro study. Cell viability was determined with the MTT assay. hoechst 33342 staining and flow cytometry were used to examine the apoptosis. The mitochondrial membrane potential (MMP) and reactive oxygen species (ROS) were measured using fluorescent dye. PGC-1α and Sirt1 levels were examined using Western blotting. Neonatal mice were given monosodium glutamate (2.5 mg/g) subcutaneously at the neck from postnatal day (PD) 7 to 13, and orally administered with AA on PD 14 daily for 30 d. The learning and memory of the mice were evaluated with the Morris water maze test. hE staining was used to analyze the pyramidal layer structure in the CA1 and CA3 regions. Results: Pretreatment of Sh-SY5Y cells with AA (0.1-100 nmol/L) attenuated toxicity induced by 10 mmol/L glutamate in a concentration-dependent manner. AA 10 nmol/L significantly decreased apoptotic cell death and reduced reactive oxygen species (ROS), stabilized the mitochondrial membrane potential (MMP), and promoted the expression of PGC-1α and Sirt1. In the mice models, oral administration of AA (100 mg/kg) significantly attenuated cognitive deficits in the Morris water maze test, and restored lipid peroxidation and glutathione and the activity of SOD in the hippocampus and cortex to the control levels. AA (50 and 100 mg/kg) also attenuated neuronal damage of the pyramidal layer in the CA1 and CA3 regions. Conclusion: AA attenuates glutamate-induced cognitive deficits of mice and protects SH-SY5Y cells against glutamate-induced apoptosis in vitro.

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Hippocampal degeneration inducing impairment of learning in rats: model of dementia?

Cited by 55 publications

References 22 publications

A structural basis for memory storage in mammals

A structural basis for memory storage in mammals

Resistance exercise reduces memory impairment induced by monosodium glutamate in male and female rats

Asiatic acid, a pentacyclic triterpene in Centella asiatica, attenuates glutamate-induced cognitive deficits in mice and apoptosis in SH-SY5Y cells

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