Age and strain differences in rat place learning and hippocampal dentate gyrus frequency-potentiation

Diana, Giovanni; Domenici, Maria Rosaria; Loizzo, Alberto; Carolis, A. Scotti de; Sagratella, S.

doi:10.1016/0304-3940(94)90618-1

Cited by 56 publications

(15 citation statements)

References 12 publications

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“…However, chronic recording studies led to the important discovery that LTP in the perforant path projections to the dentate gyrus decays more quickly in the aged brain (Barnes, 1979). Subsequent work with slices identified deficits in the induction and/or expression of LTP in field CA1 (Deupree et al, 1993;Sankar et al, 2000) while others, in agreement with the earlier studies, found no evidence for deficits in that region (Diana et al, 1994;Norris et al, 1996). It now appears that these discrepancies depend on the stimulation patterns used to induce potentiation (Moore et al, 1993;Lanahan et al, 1997;Watabe and O'Dell, 2003) and the extent to which the animals have learning problems (Tombaugh et al, 2002).…”

Section: Plasticity In Old Agementioning

confidence: 68%

Synaptic plasticity in early aging

Lynch

Rex

Gall

2006

Ageing Research Reviews

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Studies of how aging affects brain plasticity have largely focused on old animals. However, deterioration of memory begins well in advance of old age in animals, including humans; the present review is concerned with the possibility that changes in synaptic plasticity, as found in the long-term potentiation (LTP) effect, are responsible for this. Recent results indicate that impairments to LTP are in fact present by early middle age in rats but only in certain dendritic domains. The search for the origins of these early aging effects necessarily involves ongoing analyses of how LTP is induced, expressed, and stabilized. Such work points to the conclusion that cellular mechanisms responsible for LTP are redundant and modulated both positively and negatively by factors released during induction of potentiation. Tests for causes of the localized failure of LTP during early aging suggest that the problem lies in excessive activity of a negative modulator. The view of LTP as having redundant and modulated substrates also suggests a number of approaches for reversing age-related losses. Particular attention will be given to the idea that induction of brain-derived neurotrophic factor, an extremely potent positive modulator, can be used to provide long periods of normal plasticity with very brief pharmacological interventions. The review concludes with a consideration of how the selective, regional deficits in LTP found in early middle age might be related to the global phenomenon of brain aging. #

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Section: Plasticity In Old Agementioning

confidence: 68%

Synaptic plasticity in early aging

Lynch

Rex

Gall

2006

Ageing Research Reviews

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“…Other work indicates that this does not hold across all conditions (Diana et al, 1994;Norris et al, 1996) and that the presence and magnitude of deficits depends on the stimulation patterns used to induce potentiation (Moore et al, 1993;Lanahan et al, 1997;Watabe and O'Dell, 2003) and whether the animals were deficient in learning (Tombaugh et al, 2002). There appear to be no reports of impaired LTP in middle-aged rodents.…”

Section: Introductionmentioning

confidence: 99%

Long-Term Potentiation Is Impaired in Middle-Aged Rats: Regional Specificity and Reversal by Adenosine Receptor Antagonists

Rex¹,

Kramár²,

Colgin³

et al. 2005

J. Neurosci.

126

106

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Memory loss in humans begins early in adult life and progresses thereafter. It is not known whether these losses reflect the failure of cellular processes that encode memory or disturbances in events that retrieve it. Here, we report that impairments in hippocampal long-term potentiation (LTP), a form of synaptic plasticity associated with memory, are present by middle age in rats but only in select portions of pyramidal cell dendritic trees. Specifically, LTP induced with theta-burst stimulation in basal dendrites of hippocampal field CA1 decayed rapidly in slices prepared from 7-to 10-month-old rats but not in slices from young adults. There were no evident age-related differences in LTP in the apical dendrites. Both the adenosine A 1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine and a positive AMPA receptor modulator (ampakine) offset age-related LTP deficits. Adenosine produced greater depression of synaptic responses in middle-aged versus young adult slices and in basal versus apical dendrites. These results were not associated with variations in A 1 receptor densities and may instead reflect regional and age-related differences in adenosine clearance. Pertinent to this, brief applications of A 1 receptor antagonists immediately after theta stimulation fully restored LTP in middle-aged rats. We hypothesize that the build-up of extracellular adenosine during theta activity persists into the postinduction period in the basal dendrites of middle-aged slices and thereby activates the A 1 receptor-dependent LTP reversal effect. Regardless of the underlying mechanism, the present results provide a candidate explanation for memory losses during normal aging and indicate that, with regard to plasticity, different segments of pyramidal neurons age at different rates.

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“…On the contrary, the more depressed a population of synapses becomes, the more likely that subsequent stimulation will reverse the depression. The properties of LTP have been shown to depend not only on the induction protocols, but also on the time of day, and the age, strain, and species of the animal (Harris and Teyler 1983;Diana et al 1994;ManahanVaughan and Schwegler 2011;Bowden et al 2012;Cao and Harris 2012). Hence, differences in structural outcomes might arise when induction is by glutamate uncaging at individual spines versus chemical, tetanic, or TBS of multiple synapses.…”

Section: Ltp As a Model Synaptic Mechanism Contributing To Consolidatmentioning

confidence: 99%

Structural Components of Synaptic Plasticity and Memory Consolidation

Bailey

Kandel

Harris

2015

Cold Spring Harb Perspect Biol

319

259

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Consolidation of implicit memory in the invertebrate Aplysia and explicit memory in the mammalian hippocampus are associated with remodeling and growth of preexisting synapses and the formation of new synapses. Here, we compare and contrast structural components of the synaptic plasticity that underlies these two distinct forms of memory. In both cases, the structural changes involve time-dependent processes. Thus, some modifications are transient and may contribute to early formative stages of long-term memory, whereas others are more stable, longer lasting, and likely to confer persistence to memory storage. In addition, we explore the possibility that trans-synaptic signaling mechanisms governing de novo synapse formation during development can be reused in the adult for the purposes of structural synaptic plasticity and memory storage. Finally, we discuss how these mechanisms set in motion structural rearrangements that prepare a synapse to strengthen the same memory and, perhaps, to allow it to take part in other memories as a basis for understanding how their anatomical representation results in the enhanced expression and storage of memories in the brain.

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Age and strain differences in rat place learning and hippocampal dentate gyrus frequency-potentiation

Cited by 56 publications

References 12 publications

Synaptic plasticity in early aging

Synaptic plasticity in early aging

Long-Term Potentiation Is Impaired in Middle-Aged Rats: Regional Specificity and Reversal by Adenosine Receptor Antagonists

Structural Components of Synaptic Plasticity and Memory Consolidation

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