Special Issue "Molecular Regulation of Learning-induced Neuronal Plasticity"

A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Molecular and Cellular Neuroscience".

Deadline for manuscript submissions: closed (10 February 2020).

Special Issue Editors

Prof. Dr. Arturo Bevilacqua
E-Mail Website
Guest Editor
1. Department of Dynamic and Clinical Psychology and Health, Systems Biology Group Lab, Sapienza University of Rome, Research Center in Neurobiology, Daniel Bovet (CRiN), Rome, Italy
2. Experts Group on Inositol in Basic and Clinical Research, Rome, Italy
Interests: neuronal plasticity; molecular mechanisms of fear conditioning; memory formation; memory consolidation; neuronal ligand-receptor mechanisms; genetics; genomics; mammalian gametogenesis; preimplantation development; reproductive medicine; reproductive biology; assisted reproductive technology; developmental biology; ovary
Dr. David Conversi
E-Mail Website
Guest Editor
Department of Psychology, Sapienza University of Rome, and Research Center in Neurobiology, Daniel Bovet (CRiN), Rome, Italy
Interests: memory consolidation; neuronal plasticity; extinction; transcription factors; amygdala; hippocampus; prefrontal cortex; emotional arousal

Special Issue Information

Dear Colleagues,

Neuronal plasticity refers to the capacity of neurons to adapt their synaptic connections in an activity-dependent manner. This adaptation is thought to underlie both learning throughout the lifespan and functional recovery after brain lesions. In particular, for decades the experimental study of neuronal plasticity has mainly involved the electrophysiology of synapses combined with the neuropharmacology of neurotransmitters. Today, the field has dramatically expanded, and a plethora of molecules regulating neuronal plasticity both at the functional (i.e., long-term potentiation of depression) and the morphological level (i.e., dendritic spine dynamics) have been discovered.

However, despite the large body of excellent existing literature, molecular processes regulating learning-induced neuronal plasticity are not well understood. This Special Issue, therefore, focuses on review and original research articles that help gathering further details on the cellular and molecular regulation of neuronal plasticity in the hippocampus and other areas involved in the processes of memory formation and consolidation.

Dr. Arturo Bevilacqua
Dr. David Conversi
Guest Editors

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 papers will be 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. Brain Sciences is an international peer-reviewed open access monthly 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 2000 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

  • neuronal plasticity
  • synaptic plasticity
  • memory formation
  • memory consolidation
  • memory extinction
  • amygdala
  • hippocampus
  • prefrontal cortex

Published Papers (3 papers)

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Research

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Article
Sex Differences in Context-Driven Reinstatement of Methamphetamine Seeking is Associated with Distinct Neuroadaptations in the Dentate Gyrus
Brain Sci. 2018, 8(12), 208; https://doi.org/10.3390/brainsci8120208 - 28 Nov 2018
Cited by 6 | Viewed by 2596
Abstract
The present study examined differences in operant responses in adult male and female rats during distinct phases of addiction. Males and females demonstrated escalation in methamphetamine (0.05 mg/kg, i.v.) intake with females showing enhanced latency to escalate, and bingeing. Following protracted abstinence, females [...] Read more.
The present study examined differences in operant responses in adult male and female rats during distinct phases of addiction. Males and females demonstrated escalation in methamphetamine (0.05 mg/kg, i.v.) intake with females showing enhanced latency to escalate, and bingeing. Following protracted abstinence, females show reduced responses during extinction, and have greater latency to extinguish compared with males, indicating reduced craving. Females demonstrated lower context-driven reinstatement compared to males, indicating that females have less motivational significance to the context associated with methamphetamine. Whole-cell patch-clamp recordings on dentate gyrus (DG) granule cell neurons (GCNs) were performed in acute brain slices from controls and methamphetamine experienced male and female rats, and neuronal excitability was evaluated from GCNs. Reinstatement of methamphetamine seeking reduced spiking in males, and increased spiking in females compared to controls, demonstrating distinct neuroadaptations in intrinsic excitability of GCNs in males and females. Reduced excitability of GCNs in males was associated with enhanced levels of neural progenitor cells, expression of plasticity-related proteins including CaMKII, and choline acetyltransferase in the DG. Enhanced excitability in females was associated with an increased GluN2A/2B ratio, indicating changes in postsynaptic GluN subunit composition in the DG. Altered intrinsic excitability of GCNs was associated with reduced mossy fiber terminals in the hilus and pyramidal projections, demonstrating compromised neuroplasticity in the DG in both sexes. The alterations in excitability, plasticity-related proteins, and mossy fiber density were correlated with enhanced activation of microglial cells in the hilus, indicating neuroimmune responses in both sexes. Together, the present results indicate sexually dimorphic adaptive biochemical changes in excitatory neurotransmitter systems in the DG and highlight the importance of including sex as a biological variable in exploring neuroplasticity and neuroimmune changes that predict enhanced relapse to methamphetamine-seeking behaviors. Full article
(This article belongs to the Special Issue Molecular Regulation of Learning-induced Neuronal Plasticity)
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Review

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Review
Neuromodulators and Long-Term Synaptic Plasticity in Learning and Memory: A Steered-Glutamatergic Perspective
Brain Sci. 2019, 9(11), 300; https://doi.org/10.3390/brainsci9110300 - 31 Oct 2019
Cited by 14 | Viewed by 5248
Abstract
The molecular pathways underlying the induction and maintenance of long-term synaptic plasticity have been extensively investigated revealing various mechanisms by which neurons control their synaptic strength. The dynamic nature of neuronal connections combined with plasticity-mediated long-lasting structural and functional alterations provide valuable insights [...] Read more.
The molecular pathways underlying the induction and maintenance of long-term synaptic plasticity have been extensively investigated revealing various mechanisms by which neurons control their synaptic strength. The dynamic nature of neuronal connections combined with plasticity-mediated long-lasting structural and functional alterations provide valuable insights into neuronal encoding processes as molecular substrates of not only learning and memory but potentially other sensory, motor and behavioural functions that reflect previous experience. However, one key element receiving little attention in the study of synaptic plasticity is the role of neuromodulators, which are known to orchestrate neuronal activity on brain-wide, network and synaptic scales. We aim to review current evidence on the mechanisms by which certain modulators, namely dopamine, acetylcholine, noradrenaline and serotonin, control synaptic plasticity induction through corresponding metabotropic receptors in a pathway-specific manner. Lastly, we propose that neuromodulators control plasticity outcomes through steering glutamatergic transmission, thereby gating its induction and maintenance. Full article
(This article belongs to the Special Issue Molecular Regulation of Learning-induced Neuronal Plasticity)
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Other

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Opinion
Functional and Dysfunctional Neuroplasticity in Learning to Cope with Stress
Brain Sci. 2020, 10(2), 127; https://doi.org/10.3390/brainsci10020127 - 24 Feb 2020
Cited by 4 | Viewed by 2672
Abstract
In this brief review, we present evidence of the primary role of learning-associated plasticity in the development of either adaptive or maladaptive coping strategies. Successful interactions with novel stressors foster plasticity within the neural circuits supporting acquisition, consolidation, retrieval, and extinction of instrumental [...] Read more.
In this brief review, we present evidence of the primary role of learning-associated plasticity in the development of either adaptive or maladaptive coping strategies. Successful interactions with novel stressors foster plasticity within the neural circuits supporting acquisition, consolidation, retrieval, and extinction of instrumental learning leading to development of a rich repertoire of flexible and context-specific adaptive coping responses, whereas prolonged or repeated exposure to inescapable/uncontrollable stressors fosters dysfunctional plasticity within the learning circuits leading to perseverant and inflexible maladaptive coping strategies. Finally, the results collected using an animal model of genotype-specific coping styles indicate the engagement of different molecular networks and the opposite direction of stress effects (reduced vs. enhanced gene expression) in stressed animals, as well as different behavioral alterations, in line with differences in the symptoms profile associated with post-traumatic stress disorder. Full article
(This article belongs to the Special Issue Molecular Regulation of Learning-induced Neuronal Plasticity)
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