Synaptic Plasticity in Brain and Nerves: New Vistas in Health and Diseases

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: closed (30 November 2023) | Viewed by 4186

Special Issue Editor


E-Mail Website
Guest Editor
UMR-S 1075 INSERM/Unicaen (COMETE), Campus Jules Horowitz, Boulevard Henri Becquerel, 14032 Caen, France
Interests: electrophysiology; long-term potentiation; glutamate; brain diseases; aging

Special Issue Information

Dear Colleagues,

The efficiency of brain-dependent functions is closely related to optimal communication within neuronal networks, which is finely regulated by a myriad of adaptative processes involving interactions between the nerve and glial cell elements of the synaptic cleft. The capacity of brain plasticity that manages the network adaptation to environmental changes ranges from short-term modifications of cell morphology and functionality to long-term homeostatic responses. This Special Issue aims to showcase original articles and reviews that will improve our knowledge on the cellular and molecular mechanisms underlying Hebbian and homeostatic forms of synaptic plasticity. The exact nature of cellular interactions and the associated signaling pathways that contribute to the modulation of synaptic strength in cerebral networks, as well as an assessment on whether these processes are ubiquitous or show region specificity in the healthy brain remains a current topic of major interest. In addition, we welcome all articles that consider if specific alterations of synaptic adaptative processes are indicative of selective brain-related disorders that could help to initiate new preventive strategies.

Dr. Jean-Marie Billard
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • cellular networks
  • synaptic strength
  • Hebbian plasticity
  • homeostatic plasticity
  • neuron-glia interactions
  • brain disorders
  • cognitive functions

Published Papers (3 papers)

Order results
Result details
Select all
Export citation of selected articles as:

Research

0 pages, 3403 KiB  
Article
Effect of Acute Enriched Environment Exposure on Brain Oscillations and Activation of the Translation Initiation Factor 4E-BPs at Synapses across Wakefulness and Sleep in Rats
by José Lucas Santos, Evlalia Petsidou, Pallavi Saraogi, Ullrich Bartsch, André P. Gerber and Julie Seibt
Cells 2023, 12(18), 2320; https://doi.org/10.3390/cells12182320 - 20 Sep 2023
Viewed by 1236
Abstract
Brain plasticity is induced by learning during wakefulness and is consolidated during sleep. But the molecular mechanisms involved are poorly understood and their relation to experience-dependent changes in brain activity remains to be clarified. Localised mRNA translation is important for the structural changes [...] Read more.
Brain plasticity is induced by learning during wakefulness and is consolidated during sleep. But the molecular mechanisms involved are poorly understood and their relation to experience-dependent changes in brain activity remains to be clarified. Localised mRNA translation is important for the structural changes at synapses supporting brain plasticity consolidation. The translation mTOR pathway, via phosphorylation of 4E-BPs, is known to be activate during sleep and contributes to brain plasticity, but whether this activation is specific to synapses is not known. We investigated this question using acute exposure of rats to an enriched environment (EE). We measured brain activity with EEGs and 4E-BP phosphorylation at cortical and cerebellar synapses with Western blot analyses. Sleep significantly increased the conversion of 4E-BPs to their hyperphosphorylated forms at synapses, especially after EE exposure. EE exposure increased oscillations in the alpha band during active exploration and in the theta-to-beta (4–30 Hz) range, as well as spindle density, during NREM sleep. Theta activity during exploration and NREM spindle frequency predicted changes in 4E-BP hyperphosphorylation at synapses. Hence, our results suggest a functional link between EEG and molecular markers of plasticity across wakefulness and sleep. Full article
Show Figures

Graphical abstract

17 pages, 1805 KiB  
Article
Long-Term—But Not Short-Term—Plasticity at the Mossy Fiber–CA3 Pyramidal Cell Synapse in Hippocampus Is Altered in M1/M3 Muscarinic Acetylcholine Receptor Double Knockout Mice
by Fang Zheng, Jürgen Wess and Christian Alzheimer
Cells 2023, 12(14), 1890; https://doi.org/10.3390/cells12141890 - 19 Jul 2023
Viewed by 976
Abstract
Muscarinic acetylcholine receptors are well-known for their crucial involvement in hippocampus-dependent learning and memory, but the exact roles of the various receptor subtypes (M1–M5) are still not fully understood. Here, we studied how M1 and M3 receptors affect plasticity at the mossy fiber [...] Read more.
Muscarinic acetylcholine receptors are well-known for their crucial involvement in hippocampus-dependent learning and memory, but the exact roles of the various receptor subtypes (M1–M5) are still not fully understood. Here, we studied how M1 and M3 receptors affect plasticity at the mossy fiber (MF)–CA3 pyramidal cell synapse. In hippocampal slices from M1/M3 receptor double knockout (M1/M3-dKO) mice, the signature short-term plasticity of the MF–CA3 synapse was not significantly affected. However, the rather unique NMDA receptor-independent and presynaptic form of long-term potentiation (LTP) of this synapse was much larger in M1/M3-deficient slices compared to wild-type slices in both field potential and whole-cell recordings. Consistent with its presynaptic origin, induction of MF-LTP strongly enhanced the excitatory drive onto single CA3 pyramidal cells, with the effect being more pronounced in M1/M3-dKO cells. In an earlier study, we found that the deletion of M2 receptors in mice disinhibits MF-LTP in a similar fashion, suggesting that endogenous acetylcholine employs both M1/M3 and M2 receptors to constrain MF-LTP. Importantly, such synergism was not observed for MF long-term depression (LTD). Low-frequency stimulation, which reliably induced LTD of MF synapses in control slices, failed to do so in M1/M3-dKO slices and gave rise to LTP instead. In striking contrast, loss of M2 receptors augmented LTD when compared to control slices. Taken together, our data demonstrate convergence of M1/M3 and M2 receptors on MF-LTP, but functional divergence on MF-LTD, with the net effect resulting in a well-balanced bidirectional plasticity of the MF–CA3 pyramidal cell synapse. Full article
Show Figures

Figure 1

16 pages, 2913 KiB  
Article
Effects of the Light/Dark Phase and Constant Light on Spatial Working Memory and Spine Plasticity in the Mouse Hippocampus
by Jane K. Schröder, Laila Abdel-Hafiz, Amira A. H. Ali, Teresa C. Cousin, Johanna Hallenberger, Filipe Rodrigues Almeida, Max Anstötz, Maximilian Lenz, Andreas Vlachos, Charlotte von Gall and Federica Tundo-Lavalle
Cells 2023, 12(13), 1758; https://doi.org/10.3390/cells12131758 - 30 Jun 2023
Cited by 1 | Viewed by 1256
Abstract
Circadian rhythms in behavior and physiology such as rest/activity and hormones are driven by an internal clock and persist in the absence of rhythmic environmental cues. However, the period and phase of the internal clock are entrained by the environmental light/dark cycle. Consequently, [...] Read more.
Circadian rhythms in behavior and physiology such as rest/activity and hormones are driven by an internal clock and persist in the absence of rhythmic environmental cues. However, the period and phase of the internal clock are entrained by the environmental light/dark cycle. Consequently, aberrant lighting conditions, which are increasing in modern society, have a strong impact on rhythmic body and brain functions. Mice were exposed to three different lighting conditions, 12 h light/12 h dark cycle (LD), constant darkness (DD), and constant light (LL), to study the effects of the light/dark cycle and aberrant lighting on the hippocampus, a critical structure for temporal and spatial memory formation and navigation. Locomotor activity and plasma corticosterone levels were analyzed as readouts for circadian rhythms. Spatial working memory via Y-maze, spine morphology of Golgi–Cox-stained hippocampi, and plasticity of excitatory synapses, measured by number and size of synaptopodin and GluR1-immunreactive clusters, were analyzed. Our results indicate that the light/dark cycle drives diurnal differences in synaptic plasticity in hippocampus. Moreover, spatial working memory, spine density, and size and number of synaptopodin and GluR1 clusters were reduced in LL, while corticosterone levels were increased. This indicates that acute constant light affects hippocampal function and synaptic plasticity. Full article
Show Figures

Figure 1

Back to TopTop