Special Issue "Neural Mechanisms of Learning and Memory"
A special issue of Biology (ISSN 2079-7737).
Deadline for manuscript submissions: 31 August 2014
Prof. Dr. Bertram Opitz
School of Psychology, University of Surrey, Guildford, Surrey, GU2 7XH, UK
Interests: neural basis of learning and memory; long term memory formation; second language acquisition; feedback based learning
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
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. Papers will be published continuously (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as 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 refereed through a 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 300 CHF (Swiss Francs). English correction and/or formatting fees of 250 CHF (Swiss Francs) will be charged in certain cases for those articles accepted for publication that require extensive additional formatting and/or English corrections.
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: firstname.lastname@example.org (B.B.); email@example.com (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: firstname.lastname@example.org
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: Article
Title: The NF-kB transcription factor regulates Gadd45 expression and DNA demethylation during fear memory formation
Authors: Timothy J. Jarome 1, Jasmyne S. Thomas 1, Jessica N. Nichols 2, Natasha L. Pacheco 1, Rosemary E. Puckett 3, R. Ryley Parrish 1, Swati Gupta-Agarwal 1, Robin Davis 1 and Farah D. Lubin 1,*
Affiliations: 1. Department of Neurobiology, University of Alabama at Birmingham, Birmingham, AL USA; E-Mail: email@example.com
2. Department of Cell, Molecular and Developmental Biology, University of Alabama at Birmingham, Birmingham, AL USA
3. Department of Cell, Developmental and Integrative Biology, University of Alabama at Birmingham, Birmingham, AL USA
Abstract: Gadd45-mediated DNA demethylation mechanisms have been implicated in the process of memory formation. However, the transcriptional mechanisms involved in the regulation of Gadd45 gene expression during memory formation remain unexplored. NF-kB (nuclear factor kappa-light-chain-enhancer of activated B cells) controls transcription of DNA in neurons and is a critical regulator of synaptic plasticity and memory formation. In silico analysis revealed several NF-kB (p65 and cRel) consensus sequences within Gadd45 isoform (Gadd45a, Gadd45b, and Gadd45g) gene promoters. This study aimed to determine whether NF-kB activity alters Gadd45 expression and DNA demethylation during fear memory formation. We found that fear conditioning increased Gadd45a, Gadd45b and Gadd45g isoform gene expression in area CA1 of the hippocampus, which were differentially altered with NF-kB inhibition. Fear conditioning increased Gadd45b binding at the BDNF promoter associated with BDNF DNA demethylation, both of which were blocked with NF-kB inhibition. Further, learning-induced increases in Gadd45b mRNA levels were blocked in c-rel knockout mice. Conditional knockdown of p65 in area CA1of the hippocampus prevented learning-induced increases in Gadd45g mRNA levels and impaired fear memory. Together, these results support a novel transcriptional role for NF-kB in DNA demethylation in hippocampal neurons during fear memory formation through isoform-specific regulation of Gadd45 gene expression.
Last update: 25 June 2014