Thomas, Kerrie - Cardiff University - School of Biosciences

研究领域

Using contemporary techniques ranging from the genome-wide analysis of gene expression to the post-transcriptional gene silencing, my lab probes the molecular substrates of long-term memory. Focusing on hippocampal-dependent fear memory, we are particularly interested in understanding the cellular and neural processes supporting the formation of new memories and those supporting the maintenance of the memories after recall. The post-retrieval processes are not a simple recapitulation of those engaged during the consolidation of the original memory. This research will contribute to knowledge of how the brain encodes behaviorally relevant information and how it is refined by experience. This knowledge is of vital importance for understanding the basis of disorders of memory and psychiatric conditions in humans.

近期论文

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Clifton, N.et al. 2017. Schizophrenia copy number variants and associative learning. Molecular Psychiatry 22(2), pp. 178-182. (10.1038/mp.2016.227) pdf Frizzati, A.et al. 2016. Comparable reduction in ZIF268 levels and cytochrome oxidase activity in the retrosplenial cortex following mammillothalamic tract lesions. Neuroscience 330, pp. 39-49. (10.1016/j.neuroscience.2016.05.030) pdf Scholz, B.et al. 2016. The regulation of cytokine networks in hippocampal CA1 differentiates extinction from those required for the maintenance of contextual fear memory after recall. PLoS ONE 11(5), article number: e0153102. (10.1371/journal.pone.0153102) pdf Trent, S.et al. 2015. Rescue of long-term memory after reconsolidation blockade. Nature Communications 6, article number: 7897. (10.1038/ncomms8897) pdf Hall, J.et al. 2015. Genetic risk for schizophrenia: convergence on synaptic pathways Involved in plasticity. Biological Psychiatry 77(1), pp. 52-68. (10.1016/j.biopsych.2014.07.011) Barnes, P. A., Kirtley, A. and Thomas, K. L. 2012. Quantitatively and qualitatively different cellular processes are engaged in CA1 during the consolidation and reconsolidation of contextual fear memory. Hippocampus 22(2), pp. 149-171. (10.1002/hipo.20879) Amin, E.et al. 2010. Selective lamina dysregulation in granular retrosplenial cortex (area 29) after anterior thalamic lesions: an in situ hybridization and trans-neuronal tracing study in rats. Neuroscience 169(3), pp. 1255-1267. (10.1016/j.neuroscience.2010.05.055) Kirtley, A. and Thomas, K. L. 2010. The exclusive induction of extinction is gated by BDNF. Learning & Memory 17(12), pp. 612-619. (10.1101/lm.1877010) Cunha, C., Brambilla, R. and Thomas, K. L. 2010. A simple role for BDNF in learning and memory?. Frontiers in Molecular Neuroscience 3, article number: 00001. (10.3389/neuro.02.001.2010) pdf Poirier, G.et al. 2008. Anterior thalamic lesions produce chronic and profuse transcriptional deregulation in retrosplenial cortex: A model of retrosplenial hypoactivity and covert pathology. Thalamus and Related Systems 4(1), pp. 59-77. Barnes, P. and Thomas, K. L. 2008. Proteolysis of proBDNF is a key regulator in the formation of memory. PLoS ONE 3(9), article number: e3248. (10.1371/journal.pone.0003248) pdf