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02/01/2018 · Synaptic Plasticity and Memory: ..

KW - Long-term potentiation

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The synaptic plasticity and memory hypothesis - …

N2 - Aging is associated with a general decline in physiological functions including cognitive functions. Given that the hippocampus is known to be critical for certain forms of learning and memory, it is not surprising that a number of neuronal processes in this brain area appear to be particularly vulnerable to the aging process. Long-term potentiation (LTP), a form of synaptic plasticity that has been proposed as a biological substrate for learning and memory, has been used to examine age-related changes in hippocampal synaptic plasticity. A current hypothesis states that oxidative stress contributes to age-related impairment in learning and memory. This is supported by a correlation between age, memory impairment, and the accumulation of oxidative damage to cellular macromolecules. However, it also has been demonstrated that ROS are necessary components of signal transduction cascades during normal physiological processes. This review discusses the evidence supporting the dual role of reactive oxygen species (ROS) as cellular messenger molecules in normal LTP, as well their role as damaging toxic molecules in the age-related impairment of LTP. In addition, we will discuss parallel analyses of LTP and behavioral tests in mice that overexpress antioxidant enzymes and how the role of antioxidant enzymes and ROS in modulating these processes may vary over the lifespan of an animal.

For this reason it is widely believed that synaptic plasticitymediates learning and memory.

Neuroscientists rightly honour Ramón y Cajal, but they also look upon Donald Hebb as a visionary with his ideas about the physiological circumstances in which potentiation would occur and his concept of the ‘cell-assembly’. Cooke and co-worker [] revisit the very area of the brain that Hebb had in mind, the visual cortex, and present evidence that both LTD (during the developmental fine-tuning of connections) and LTP (in the form of selective response potentiation and perceptual learning) play an important role. However, they qualify their assertion by noting that a full understanding of the role of plasticity in visual cortex will require an appreciation of intrinsic microcircuits in which other forms of plasticity may prevail.

Box 3 | Hippocampal synaptic plasticity and memory

The hypothesis that synapses store memories by modifying their strengths raisesan important issue.

Our discussion thus far has focused on the role of sleep as a major organizer of synapse and circuit plasticity in the brain. In this role, sleep acts in synchrony with the circadian rhythm to normalize, modulate, and optimize the synaptic function and circuit connectivity of cortical and subcortical neural networks. The dark side of sleep’s importance for synapse and circuit function is that sleep dysfunction is also connected to numerous neurological and neurodevelopment disorders, (), as discussed below.

So, with the experimental knowledge gathered to date from memory consolidation, visual cortex wiring, and synaptic homeostasis studies, it is safe to acknowledge that sleep, on a synaptic level, is a specific type of plastic state likely conserved across circuits, developmental stages, and evolution. This critical state is not only important for the proper function of the nervous system, but is itself dependent on the prior activity and connectivity of the nervous system. While the effects of sleep on synaptic plasticity during normal physiological conditions will require extensive studies for many years to come, pathological conditions such as observed in neurodegenerative and neurodevelopmental disorders should also shed light on the association of abnormal sleep and cognition impairment.

Synaptic plasticity, memory and the hippocampus: a …

Thus both depotentiation and LTD can support recognition memory, at least in the longer term.

Not only can LTD provide a sound mechanistic solution to neuronal decrement, the regulation of input specificity means that, under normal conditions, only single synapses undergo modification from each incoming signal.

A hypothetical model for the role of HDAC2 in transcriptional repression of synaptic plasticity genes in neuronal cells infected with HIV and/or in the presence of nicotine. During the gene transcription, the DNA to be transcribed is associated with histone proteins (blue) that are modified by the addition of acetyl groups (green). This modification results in a relaxed chromatin configuration that allows the transcriptional machinery access to the DNA. Up-regulation of HDAC2 during HIV infection and/or nicotine treatment leads to deletion of acetyl groups from histone proteins, resulting in a condensed chromatin that limits the binding of the transcriptional machinery, thereby decreasing gene transcription. Thus, inhibition of HDAC2 by using vorinostat may block these enzymatic processes and return the chromatin to a relaxed state, allowing gene transcription.

Most of the current knowledge on learning and initial stages of memory consolidation (“synaptic consolidation”) is based on this hypothesis.
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  • Memory stability and synaptic plasticity - DSpace Home

    This synaptic plasticity is bidirectional and synapsescan be strengthened (potentiation) or weakened (depression).

  • Memory, Synaptic Plasticity, ..

    If the synaptic plasticity genes expression change is ± ≥3 fold, the fold change was represented in bold letters.

  • Synaptic plasticity | Psychology Wiki | FANDOM …

    the synaptic plasticity and memory hypothesis states that “activity-dependent synaptic plasticity is induced at ..

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For the general concept of brain plasticity, see neuroplasticity

Tonegawa et al. [] take to the field in the exciting new territory of false memory. It has long been known that memory is not always veridical and that people may, under certain circumstances, believe that something happened in the past when in fact it did not. This is an interesting test case of the synaptic plasticity and memory idea as the ability of multiple synaptic changes to ‘mimic’ a memory would satisfy an important prediction of the hypothesis. The Tonegawa group goes on to describe how they have used optogenetics in conjunction with context fear conditioning to train animals to behave as afraid in a neutral situation in which nothing untoward has happened. Their paper describes how the intellectual context of their work is very much in the spirit of identifying and manipulating hippocampal engrams, as outlined by Mayford, although both approaches involve direct manipulation of cells rather than synapses.

Hippocampal synaptic plasticity, spatial memory and anxiety.

One area of controversy highlighted by Mayford concerns the role that NMDA receptors may play in learning. An early idea was that, in hippocampus, they would be crucial functionally because they would provide the mechanism of signalling an association between pre- and postsynaptic activity, so providing a molecular basis for Hebbian synaptic plasticity. New work by Bannerman and co-workers [] using mutant mice questions this assumption, with data suggesting that spatial learning can be quite normal in animals with GluN1 deleted in CA1 and the dentate gyrus—though these mice do show a deficit in spatial reversal learning. They suggest that ‘hippocampal NMDARs, particularly in CA1, act as part of a comparator system to detect and resolve conflicts arising when two competing, behavioural response options are evoked concurrently, through activation of a behavioural inhibition system’. Bannerman and Morris, using pharmacological techniques, had in earlier work together raised the question of whether NMDA receptors are necessary for long-term spatial learning. Their views have now diverged with Bannerman raising the idea of a role in selecting between different behavioural outputs, while Morris asserts that NMDA receptors are vital and that the critical role of CA1 and CA3 NMDA receptors is in enabling one-shot episodic-like memory encoding.

Synaptic Plasticity and Memory Formation

Wang and co-workers [] also provide a fresh perspective on an old problem. It has long been appreciated that a memory trace may be formed but that is no guarantee that it will last, leading to the many studies of ‘consolidation’. This is the process that somehow stabilizes memory traces. The lateral thinking they bring to this issue is to raise the spectre that forgetting itself may not be a passive process, but one involving the active removal of AMPA receptors from the postsynaptic density. Focusing here on early- and late-LTP, they provide evidence that even consolidated changes in synaptic potentiation (i.e. late-LTP) can be subjected to active forgetting and that blocking the process of AMPA receptor endocytosis can make potentiation last longer. It will be interesting to see whether the same intervention prolongs memories.

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