Aging and Synaptic Plasticity: A Review

Bergado, Jorge A.; Almaguer, William

doi:10.1155/np.2002.217

Cited by 50 publications

(27 citation statements)

References 181 publications

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“…It is possible that exploration of novel environments during aging may facilitate DG LTP by increasing dopaminergic, cholinergic, or adrenergic neurotransmission. However, all these systems are negatively affected during aging (Luine et al, 1990;Chouinard et al, 1995;Stemmelin et al, 2000) and the facilitation of LTP by dopaminergic (Bach et al, 1999), cholinergic (Frey et al, 2001;Bergado and Almaguer, 2002), and adrenergic (Seidenbecher et al, 1997;Bergado and Almaguer, 2002) inputs are impaired during aging and thus are unlikely to facilitate DG LTP during exploration of novel environments. Further studies will be required to definitively identify the neuromodulators involved in the novelty-mediated enhancement of DG LTP during aging.…”

Section: Discussionmentioning

confidence: 99%

Brief novelty exposure facilitates dentate gyrus LTP in aged rats

2008

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Aging is associated with a decreased capacity for dentate gyrus (DG) granule cell depolarization as well as reduced perforant path activation. Although it is well established that the maintenance of DG long-term potentiation (LTP) over days is impaired in aged, as compared to young animals, the threshold for inducing this LTP has never been investigated in aged, awake animals. In addition, although exposure to novelty prior to θ-burst stimulation (TBS) increases both the induction and longevity of DG LTP in adult rats, the effects of exposure to novelty on LTP in aged rats have never been investigated. Here, we report that although TBS delivered in the home cage induces robust and long-lasting DG LTP in young rats, TBS fails to induce DG LTP in aged rats. Interestingly, delivery of TBS to aged rats exploring novel environments induces robust and longlasting LTP, with the induction, but not the longevity, of this LTP being similar in magnitude to that observed in young rats delivered TBS in the home cage. These results indicate that although TBS-induced DG LTP is impaired in aged, as compared to young rats, TBS during exploration of novel environments is sufficient to rescue age-related deficits in DG LTP. We discuss these observations in the context of previous findings suggesting that the facilitation of LTP by exposure to novel environments results as a consequence of reduced network inhibition in the DG and we suggest that, in spite of age-related changes in the DG, this capacity persists in aged rats and represents a nondietary and nonpharmacological way to facilitate DG LTP during aging.

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Section: Discussionmentioning

confidence: 99%

Brief novelty exposure facilitates dentate gyrus LTP in aged rats

2008

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“…Concerning cognitive disabilities, our study shows that their prevalence increases with age, markedly so after 70 years, for concentration-attention, orientation, problem-solving, and memory. The alterations in cognitive function in the elderly can be caused by atrophy in certain cortical areas [35] or the hippocampus [36] and by modifi cation in neural plasticity [37] .…”

Section: Discussionmentioning

confidence: 99%

Prevalence of Sensory and Cognitive Disabilities and Falls, and Their Relationships: A Community-Based Study

Gauchard

Deviterne²,

Guillemin³

et al. 2006

Neuroepidemiology

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This study assessed the prevalence of sensory and cognitive disabilities and falls for various age groups, sexes, and socio-occupational categories, and their associations in the Lorraine population.The sample included6,159 subjects, aged 15 years or more, randomly selected from the Lorraine population. They filled in a mailed questionnaire including socio-demographic characteristics, job, falls with physical injuries at the time of the survey, and sensory and cognitive disabilities. Data analysis was made via the adjusted odds ratios.The prevalences of sensory and cognitive disabilities were 3.0 and 4.7%, respectively, that of falls with physical injuries 2.4%: 1.2% for falls on the same level and 1.2% for falls to a lower level. Subjects aged over 70 were markedly affected, but the other age groups had relatively high prevalences as well; the workmen had the highest prevalence, followed by the foremen, farmers, craftsmen and tradesmen, and employees. A twofold risk independently of age, sex and job was found for the subjects with sensory or cognitive disabilities for all falls combined.These findings show the high prevalences of sensory and cognitive disabilities and falls with physical injuries, and their strong associations in the general population. Preventive measures are needed to detect and follow up the persons with these disabilities, limit their risk of falls and reduce occupational hazards.

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“…Reversal of aging-related deficits in NMDARmediated synaptic plasticity by acute treatment with reductants that can affect thiol redox status directly A number of studies have identified that synaptic plasticity deficits in hippocampal circuits of aged rats have a pronounced impact on their learning and memory (deToledo-Morrell et al, 1988;Bergado & Almaguer, 2002). Consistent with previous reports, a significant suppression of NMDAR-dependent LTP in aged rat hippocampus was observed compared with adult rats in this study (adult rat 143.3 ± 15.3%; aged rat 110.1 ± 13.8%, P < 0.05 vs. adult rat, Fig.…”

Section: Modulation Of Thiol Redox Status Affects Nmdarmediated Synapmentioning

confidence: 99%

Reversal of aging‐associated hippocampal synaptic plasticity deficits by reductants via regulation of thiol redox and NMDA receptor function

Yang

Long

et al. 2010

Aging Cell

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SummaryDeficits in learning and memory accompanied by agerelated neurodegenerative diseases are closely related to the impairment of synaptic plasticity. In this study, we investigated the role of thiol redox status in the modulation of the N-methyl-D-aspartate receptor (NMDAR)-dependent long-term potentiation (LTP) in CA1 areas of hippocampal slices. Our results demonstrated that the impaired LTP induced by aging could be reversed by acute administration of reductants that can regulate thiol redox status directly, such as dithiothreitol or b-mercaptoethanol, but not by classical anti-oxidants such as vitamin C or trolox. This repair was mediated by the recruitment of aging-related deficits in NMDAR function induced by these reductants and was mimicked by glutathione, which can restore the age-associated alterations in endogenous thiol redox status. Moreover, antioxidant prevented but failed to reverse H 2 O 2 -induced impairment of NMDARmediated synaptic plasticity. These results indicate that the restoring of thiol redox status may be a more effective strategy than the scavenging of oxidants in the treatment of pre-existing oxidative injury in learning and memory.

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Aging and Synaptic Plasticity: A Review

Cited by 50 publications

References 181 publications

Brief novelty exposure facilitates dentate gyrus LTP in aged rats

Brief novelty exposure facilitates dentate gyrus LTP in aged rats

Prevalence of Sensory and Cognitive Disabilities and Falls, and Their Relationships: A Community-Based Study

Reversal of aging‐associated hippocampal synaptic plasticity deficits by reductants via regulation of thiol redox and NMDA receptor function

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