Clarrisa A. Bradley
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Clarrisa A. Bradley has a total of 9 co-authors. Here are the top co-authors by number of shared publications:
- Bong-Kiun Kaang
School of Biological Sciences, Seoul National University
1 shared publication - Celine S. Nicolas
Centre for Synaptic Plasticity, School of Physiology, Pharmacology & Neuroscience, University of Bristol, Bristol, UK
1 shared publication - Changiz Taghibiglou
Department of Pharmacology, College of Medicine, University of Saskatchewan, Saskatoon SK, Canada
1 shared publication - Daniel J. Whitcomb
School of Psychology and Neuroscience, University of Bristol, Bristol BS8 1TD, UK
1 shared publication - Graham L. Collingridge
Center for Synaptic Plasticity, School of Physiology and Pharmacology, University of Bristol, United Kingdom
1 shared publication - Kwangwook Cho
Department of Basic and Clinical Neuroscience, Institute of Psychiatry, Psychology and Neuroscience, King’s College London, London, UK
1 shared publication
Latest Publications
- Open Access
- 1 January 2012
- Published by Frontiers Media SA in Frontiers in Molecular Neuroscience
- Vol. 5, 13
A pivotal role of GSK-3 in synaptic plasticity
Glycogen synthase kinase-3 (GSK-3) has many cellular functions. Recent evidence suggests that it plays a key role in certain types of synaptic plasticity, in particular a form of long-term depression (LTD) that is induced by the synaptic activation of N-methyl-D-aspartate receptors (NMDARs). In the present article we summarize what is currently known concerning the roles of GSK-3 in synaptic plasticity at both glutamatergic and GABAergic synapses. We summarize its role in cognition and speculate on how alterations in the synaptic functioning of GSK-3 may be a major factor in certain neurodegenerative disorders.
- 1 January 2012
- Published by Frontiers Media SA in Frontiers in Molecular Neuroscience
- Vol. 5, 13
Open AccessA pivotal role of GSK-3 in synaptic plasticity
Glycogen synthase kinase-3 (GSK-3) has many cellular functions. Recent evidence suggests that it plays a key role in certain types of synaptic plasticity, in particular a form of long-term depression (LTD) that is induced by the synaptic activation of N-methyl-D-aspartate receptors (NMDARs). In the present article we summarize what is currently known concerning the roles of GSK-3 in synaptic plasticity at both glutamatergic and GABAergic synapses. We summarize its role in cognition and speculate on how alterations in the synaptic functioning of GSK-3 may be a major factor in certain neurodegenerative disorders.