Special Issue "Neural Mechanisms of Learning and Memory"
A special issue of Biology (ISSN 2079-7737).
Deadline for manuscript submissions: closed (31 August 2014)
Our brains hold a seemingly endless amount of information, from childhood memories to our home addresses. Not only neuroscience is already attempting to answer the question how are we able to learn, store, and recall all this information with such ease?
In a special issue of Biology we are going to rely on the huge range of concepts and techniques, from molecular events in the nervous system and human system neuroscientific approaches, to computational models aiming at a holistic picture of the neural mechanisms involved.
Advances in molecular biology and genetics are offering new clues about key molecules and proteins that influence memory. Research at the cellular level has shown that brain cells undergo chemical and structural changes during learning by changing the number or strength of connections between themselves. Recent animal studies suggest that manipulating these molecules could lead to new ways of modifying memories. Other studies on human participants have attempted to identify how different areas of the brain work together to enhance memory formation and storage.
For this special issue of Biology, we invite research articles from any field of neuroscience to help expand our understanding of the neural mechanisms of learning and memory.
Prof. Dr. Bertram Opitz
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. Biology is an international peer-reviewed open access quarterly 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 650 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.
The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.
Type of Paper: Article
Title: Interacting memory systems - does EEG alpha activity respond to semantic long-term memory access in a working memory task?
Authors: Barbara Berger, Serif Omer, Annette Sterr and Paul Sauseng
Affiliation: School of Psychology, Faculty of Arts and Human Sciences, University of Surrey, Guildford GU2 7XH, UK; E-Mails: email@example.com (B.B.); firstname.lastname@example.org (P.S.)
Abstract: Memory consists of various individual processes which form a dynamic system co-ordinated by central (executive) functions. The episodic buffer as direct interface between episodic long-term memory (LTM) and working memory (WM) is fairly well studied but such direct interaction is less clear in semantic LTM. Here we designed a verbal late-match-to-sample task specifically to differentiate between pure information maintenance and mental manipulation of memory traces with and without involvement of access to semantic LTM. Task-related amplitude differences of electroencephalographic (EEG) oscillatory brain activity showed a linear increase in frontal-midline theta and linear suppression of parietal beta amplitudes relative to memory operation complexity. Amplitude suppression at fast alpha frequency, which was previously found to indicate access to semantic LTM, was only sensitive to mental manipulation in general, irrespective of LTM involvement.
This suggests that suppression of fast EEG alpha activity might rather reflect unspecific distributed cortical activation during complex mental processes than accessing semantic LTM.
Type of Paper: Article
Title: Effects of anodal transcranial Direct Current Stimulation on visuo-motor learning
Authors: Tamas Minarik, Paul Sauseng and Annette Sterr
Affiliation: Brain and Behaviour Research Group, School of Psychology, University of Surrey, UK; E-Mail: email@example.com
Abstract: Anodal transcranial Direct Current Stimulation (anodal-tDCS) has been shown to be an effective non-invasive brain stimulation method for improving cognitive and motor functioning in patients with neurological deficits. Anodal-tDCS over motor cortex, for instance, facilitates motor learning in stroke patients. However, findings on the effects of motor cortex anodal-tDCS on motor learning in healthy participants are inconclusive. Furthermore, its effect on visuo-motor integration is not well understood. In the present study we examined whether anodal-tDCS over the motor cortex enhances visuo-motor learning in a power-grip task in a healthy population. Participants completed a 2-session protocol with 40 minutes power-grip task in each session. This task required the control of a visual signal by modulating the strength of the power-grip for 6 seconds per trial and was carried out under anodal-tDCS and sham condition for each participant. The neurosimulation protocol comprised a standard montage with the active electrode over the contralateral motor cortex and 20 minutes of 1mA stimulation or sham stimulation (counterbalanced), with a week apart. Performance measures derived from time-on-target and target-deviation showed significant improvement over time for both stimulation conditions; during and after anodal-tDCS. Importantly, however, the results suggest that the applied neurostimulation did not influence visuo-motor learning. Specifically, anodal-tDCS had an impact neither within session nor between sessions (consolidation) on these performance measures. These findings in combination with previous studies indicate that anodal-tDCS improvements might be limited to cases where the motor system is challenged, i.e. patients with motor deficits or situations of very high task demand.
Type of Paper: Review
Title: Environmental enrichment reverses age-related changes in histone methylation levels in the hippocampus during memory consolidation
Authors: Sarah J. Morse, Robin L. Davis, Anderson A. Butler, Ian J. Soller, Jasmyne S. Thomas and Farah D. Lubin*
Affiliation: The Evelyn F. McKnight Brain Institute, Department of Neurobiology, University of Alabama at Birmingham, 1825 University Boulevard, Birmingham, AL 35294, USA; E-Mail: firstname.lastname@example.org
Abstract: Age-related memory decline is associated with gene expression changes in the hippocampus. Histone methylation-mediated gene transcription in the hippocampus is necessary for memory formation. Here we found that resting histone H3 lysine 4 trimethylation (H3K4me3) and H3 lysine 9 dimethylation (H3K9me2) levels increased in the aged hippocampus. We found that with increased H3K9me2, histone H3 lysines 9 and 14 acetylation was significantly decreased in the aged hippocampus. Inhibition of the histone demethylase LSD1 reproduced age-related changes in H3K4me3, but not H3K9me2, levels in area CA1 of young adults, which was associated with memory impairments. We found that environmental enrichment (EE) rescued deficits in brain derived neurotrophic factor (Bdnf) but not Zif268 gene expression in area CA1 of aged adults along with H3K9me2 levels at the Bdnf promoter. Together, these results suggest that histone methylation dysregulation in the hippocampus contributes to age-related memory decline and identify histone methylation as a transcriptional mechanism by which EE may serve to restore memory function with aging.