Professor Roland Jones
Profile
Our research focuses on the control of synchrony in neuronal networks of temporal lobe brain structures. In particular we are interested in how network activity is altered in hypersynchronous states, particularly in epilepsy, and how abnormal network activity in epilepsy may be repaired by anticonvulsant drugs.
Within cortical networks, excitatory synaptic transmission is mediated by the amino acid glutamate and inhibition by gamma-aminobutyric acid (GABA). Both transmitters are released spontaneously from presynaptic nerve terminals, and provide a continuous level of background synaptic "noise" in postsynaptic neurones. It is becoming clear that this background noise is not spurious, but is functional in setting the level of excitability of neurones and, therefore, the processing capabilities of the network. We are investigating spontaneous background synaptic noise from two standpoints: (1) Using a mathematical model to derive synaptic conductances from membrane potential fluctuations, we are quantifying background inhibition and excitation, and how the balance between them determines the excitability of individual neurones (see below); (2) We are examining how the spontaneous presynaptic release of both GABA and glutamate is controlled by feedback interactions of the two transmitters with receptors on the presynaptic terminals. In particular we are studying how presynaptic ionotropic kainate and NMDA receptors modify release.
Experiments are conducted in in vitro cortical brain slice preparations from rat brain using electrophysiological approaches (intra and extracellular recording, whole cell patch clamp). With our interest in epilepsy we have previously compared network activity in tissue from normal animals and from chronically epileptic animals. A recent and novel approach in the laboratory has been to develop a new model of epilepsy induced entirely in vitro in slice preparations from rat brain maintained in culture for periods of weeks to months. This work has been funded by the National Centre for Reduction, Refinement and Replacement of animals in research and has the potential to reduce animal usage for basic epilepsy research by 80-90%.
For more information on neuroscience research at the University of Bath see http://www.bath.ac.uk/neuroscience/
Publications
Chamberlain, S. E. L., Jane, D. E. and Jones, R. S. G., 2012. Pre- and post-synaptic functions of kainate receptors at glutamate and GABA synapses in the rat entorhinal cortex. Hippocampus, 22 (3), pp. 555-576.
Greenhill, S. D., Morgan, N. H., Massey, P. V., Woodhall, G. L. and Jones, R. S. G., 2012. Ethosuximide modifies network excitability in the rat entorhinal cortex via an increase in GABA release. Neuropharmacology, 62 (2), pp. 807-814.
Greenhill, S. D. and Jones, R. S. G., 2010. Diverse antiepileptic drugs increase the ratio of background synaptic inhibition to excitation and decrease neuronal excitability in neurons of the rat entorhinal cortex in vitro. Neuroscience, 167 (2), pp. 456-474.
Yang, J., Chamberlain, S. E. L., Woodhall, G. L. and Jones, R. S. G., 2008. Mobility of NMDA autoreceptors but not postsynaptic receptors at glutamate synapses in the rat entorhinal cortex. The Journal of Physiology, 586 (20), pp. 4905-4924.
Chapman, C. A., Jones, R. S. G. and Jung, M., 2008. Neuronal plasticity in the entorhinal cortex. Neural Plasticity, 2008, 314785.
Curia, G., Longo, D., Biagini, G., Jones, R. S. G. and Avoli, M., 2008. The pilocarpine model of temporal lobe epilepsy. Journal of Neuroscience Methods, 172 (2), pp. 143-157.
Chamberlain, S. E. L., Yang, J. and Jones, R. S. G., 2008. The role of NMDA receptor subtypes in short-term plasticity in the rat entorhinal cortex. Neural Plasticity, 2008, 872456.
