Synaptic changes induced by neural activity need to be consolidated to maintain memory over a timescale of hours. In experiments, synaptic consolidation can be induced by repeating a stimulation protocol several times and the effectiveness of consolidation depends crucially on the repetition frequency of the stimulations. We address the question: is there an understandable reason why induction protocols with repetitions at some frequency work better than sustained protocols-even though the accumulated stimulation strength might be exactly the same in both cases? In real synapses, plasticity occurs on multiple time scales from seconds (induction), to several minutes (early phase of long-term potentiation) to hours and days (late phase of synaptic consolidation). We use a simplified mathematical model of just two times scales to elucidate the above question in a purified setting. Our mathematical results show that, even in such a simple model, the repetition frequency of stimulation plays an important role for the successful induction, and stabilization, of potentiation.
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http://dx.doi.org/10.3389/fncom.2019.00078 | DOI Listing |
Netw Neurosci
December 2024
Department of Cognition, Development and Education Psychology, University of Barcelona, Barcelona, Spain.
Memories are thought to use coding schemes that dynamically adjust their representational structure to maximize both persistence and efficiency. However, the nature of these coding scheme adjustments and their impact on the temporal evolution of memory after initial encoding is unclear. Here, we introduce the Segregation-to-Integration Transformation (SIT) model, a network formalization that offers a unified account of how the representational structure of a memory is transformed over time.
View Article and Find Full Text PDFJ Comput Neurosci
December 2024
Department of Physics, Drexel University, 3141 Chestnut Street, Philadelphia, 19104, PA, USA.
Traveling waves of neuronal spiking activity are commonly observed across the brain, but their intrinsic function is still a matter of investigation. Experiments suggest that they may be valuable in the consolidation of memory or learning, indicating that consideration of traveling waves in the presence of plasticity might be important. A possible outcome of this consideration is that the synaptic pathways, necessary for the propagation of these waves, will be modified by the waves themselves.
View Article and Find Full Text PDFNeuroscience
December 2024
Laboratory of Pharmacological and Toxicological Evaluations Applied to Bioactive Molecules (LaftamBio), Department of Nutrition - Federal University of Pampa, Itaqui, RS, 97650-000, Brazil.
Hypothyroidism is known to affect memory consolidation, and our prior research highlighted the potential of chrysin as a therapeutic agent to restore cognitive function. The present study aimed to investigate the action mechanism of chrysin on memory deficits in hypothyroid in C57BL/6 female mice. We assessed cognitive flexibility, declarative, working, and aversive memories while analyzing the BDNF/TrkB/AKT/Creb neuroplasticity signaling pathway and synaptic function in the hippocampus and prefrontal cortex.
View Article and Find Full Text PDFActa Neuropathol Commun
December 2024
Department of Anatomy and Neurobiology, School of Medicine, University of California, Irvine, USA.
Cranial radiation therapy (RT) for brain cancers is often associated with the development of radiation-induced cognitive dysfunction (RICD). RICD significantly impacts the quality of life for cancer survivors, highlighting an unmet medical need. Previous human studies revealed a marked reduction in plasma brain-derived neurotrophic factor (BDNF) post-chronic chemotherapy, linking this decline to a substantial cognitive dysfunction among cancer survivors.
View Article and Find Full Text PDFJ Physiol
December 2024
Department of Neuroscience and Pharmacology, The University of Iowa, Iowa City, IA, USA.
cAMP signalling is critical for memory consolidation and certain forms of long-term potentiation (LTP). Phosphodiesterases (PDEs), enzymes that degrade the second messengers cAMP and cGMP, are highly conserved during evolution and represent a unique set of drug targets, given the involvement of these enzymes in several pathophysiological states including brain disorders. The PDE4 family of cAMP-selective PDEs exert regulatory roles in memory and synaptic plasticity, but the specific roles of distinct PDE4 isoforms in these processes are poorly understood.
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