Selective reduction of hippocampal dentate frequency potentiation in aged rats with impaired place learning

Diana, Giovanni; Carolis, A. Scotti de; Frank, Claudio; Domenici, Maria Rosaria; Sagratella, S.

doi:10.1016/0361-9230(94)90089-2

Cited by 36 publications

(13 citation statements)

References 13 publications

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“…Using high-frequency stimulation, we found that the induction and maintenance of CA1 LTP were not affected by age. In agreement with our findings, previous studies have also demonstrated that if LTP is induced by high frequency and high current, the age-related impairment in the LTP inductions become undetectable [7, 37, 38]. …”

Section: Discussionsupporting

confidence: 81%

Long-Term Moderate Exercise Rescues Age-Related Decline in Hippocampal Neuronal Complexity and Memory

Tsai

Wang

et al. 2018

Gerontology

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Background: Aging impairs hippocampal neuroplasticity and hippocampus-related learning and memory. In contrast, exercise training is known to improve hippocampal neuronal function. However, whether exercise is capable of restoring memory function in old animals is less clear. Objective: Here, we investigated the effects of exercise on the hippocampal neuroplasticity and memory functions during aging. Methods: Young (3 months), middle-aged (9–12 months), and old (18 months) mice underwent moderate-intensity treadmill running training for 6 weeks, and their hippocampus-related learning and memory, and the plasticity of their CA1 neurons was evaluated. Results: The memory performance (Morris water maze and novel object recognition tests), and dendritic complexity (branch and length) and spine density of their hippocampal CA1 neurons decreased as their age increased. The induction and maintenance of high-frequency stimulation-induced long-term potentiation in the CA1 area and the expressions of neuroplasticity-related proteins were not affected by age. Treadmill running increased CA1 neuron long-term potentiation and dendritic complexity in all three age groups, and it restored the learning and memory ability in middle-aged and old mice. Furthermore, treadmill running upregulated the hippocampal expressions of brain-derived neurotrophic factor and monocarboxylate transporter-4 in middle-aged mice, glutamine synthetase in old mice, and full-length TrkB in middle-aged and old mice. Conclusion: The hippocampus-related memory function declines from middle age, but long-term moderate-intensity running effectively increased hippocampal neuroplasticity and memory in mice of different ages, even when the memory impairment had progressed to an advanced stage. Thus, long-term, moderate intensity exercise training might be a way of delaying and treating aging-related memory decline.

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Section: Discussionsupporting

confidence: 81%

Long-Term Moderate Exercise Rescues Age-Related Decline in Hippocampal Neuronal Complexity and Memory

Tsai

Wang

et al. 2018

Gerontology

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“…Similar to what is observed in CA3, LTP decays more rapidly over days in the dentate gyrus of old rats [left panel; 29]. When weak (peri-threshold) stimulation protocols are used, however, aged rats also show LTP induction deficits at the perforant path dentate gyrus synapse [right panel; 42, 43]. This induction impairment could, in part, result from the higher threshold in LTP induction at this synapse [80].…”

Section: Figurementioning

confidence: 67%

“…Even under these conditions, however, aged rats have deficits in the maintenance of LTP in both the dentate gyrus [29] and CA3 [40]. When weaker stimulation protocols are used to induce LTP, aged rats do show induction deficits in both the dentate gyrus [42, 43] and in CA1 [for review, see 4, 11]. Finally, although the maximal capacity for LTD is unaffected by aging at the Schaffer collateral–CA1 synapse [16, 44], aged rats are more susceptible to LTD induction and LTP reversal at this synapse [45].…”

Section: Summary Of Age-related Changes At Excitatory Hippocampal Synmentioning

confidence: 99%

Senescent synapses and hippocampal circuit dynamics

Burke

Barnes

2010

Trends in Neurosciences

173

152

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Excitatory synaptic transmission is altered during aging in hippocampal granule cells, and in CA3 and CA1 pyramidal cells. These functional changes contribute to age-associated impairments in experimentally-induced plasticity in each of these primary hippocampal subregions. In CA1, plasticity that is evoked by stimulation shares common mechanisms with the synaptic modification observed following natural behavior. Aging results in deficits in both artificially- and behaviorally-induced plasticity, which may in part reflect age-related changes in Ca2+ homeostasis. Other observations, however, suggest that increased intracellular Ca2+ levels are beneficial under some circumstances. This review focuses on age-associated changes in synaptic function, how these alterations may contribute to cognitive decline, and the extent to which altered hippocampal circuit properties are detrimental or reflect compensatory processes.

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“…Senescent physiology, including altered hippocampal synaptic plasticity, is thought to contribute to the decline in cognitive function associated with aging and age--associated neurodegenerative diseases (Barnes, 1979, 2003; Disterhoft et al, 1994; Lynch, 1998a; Rosenzweig and Barnes, 2003; Tombaugh et al, 2005; Disterhoft and Oh, 2006; Foster and Kumar, 2007; Lister and Barnes, 2009). In general, no age-related differences are observed in the magnitude of LTP (Landfield et al, 1978; Barnes, 1979; Deupree et al, 1993; Moore et al, 1993; Diana et al, 1994a; Norris et al, 1996; Shankar et al, 1998), however, aging is associated with a shift in synaptic plasticity favoring decreased synaptic transmission and a reduced ability to induce LTP (Landfield and Lynch, 1977; Landfield et al, 1978; Barnes, 1979, 1990, 1994; de Toledo-Morrell and Morrell, 1985; Davis et al, 1993; Deupree et al, 1993; Moore et al, 1993; Lynch and Voss, 1994; Auerbach and Segal, 1997; Lynch, 1997, 1998a,b; McGahon et al, 1997; Murray and Lynch, 1998a,b; Shankar et al, 1998; Hsu et al, 2002; Watson et al, 2002, 2006; Blank et al, 2003; Rosenzweig and Barnes, 2003; Watabe and O'Dell, 2003; Griffin et al, 2006; Kelly et al, 2011b). It has been suggested that impairment of LTP may begin in middle age (Rex et al, 2005) and a shift in synaptic plasticity, favoring LTD over LTP, contributes to the decrease in synaptic transmission observed in aged animals (Foster, 1999).…”

Section: Ltp During Agingmentioning

confidence: 99%

Long-Term Potentiation at CA3–CA1 Hippocampal Synapses with Special Emphasis on Aging, Disease, and Stress

Kumar¹

2011

Front. Ag. Neurosci.

125

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Synaptic plasticity in the mammalian central nervous system has been the subject of intense investigation for the past four decades. Long-term potentiation (LTP), a major reflection of synaptic plasticity, is an activity-driven long-lasting increase in the efficacy of excitatory synaptic transmission following the delivery of a brief, high-frequency train of electrical stimulation. LTP is regarded as a principal candidate for the cellular mechanisms involved in learning and offers an attractive hypothesis of how memories are constructed. There are a number of exceptional full-length reviews published on LTP; the current review intends to present an overview of the research findings regarding hippocampal LTP with special emphasis on aging, diseases, and psychological insults.

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Selective reduction of hippocampal dentate frequency potentiation in aged rats with impaired place learning

Cited by 36 publications

References 13 publications

Long-Term Moderate Exercise Rescues Age-Related Decline in Hippocampal Neuronal Complexity and Memory

Long-Term Moderate Exercise Rescues Age-Related Decline in Hippocampal Neuronal Complexity and Memory

Senescent synapses and hippocampal circuit dynamics

Long-Term Potentiation at CA3–CA1 Hippocampal Synapses with Special Emphasis on Aging, Disease, and Stress

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