Department of Pharmacy and Pharmacology


7 West - 3.13a


Tel: +44 (0)1225 383935


Professor Roland Jones 


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


Modebadze, T., Morgan, N. H., Pérès, I. A. A., Hadid, R. D., Amada, N., Hill, C., Williams, C., Stanford, I. M., Morris, C. M., Jones, R. S. G., Whalley, B. J. and Woodhall, G. L., 2016. A low mortality, high morbidity reduced intensity status epilepticus (RISE) model of epilepsy and epileptogenesis in the rat. PLoS ONE, 11 (2), e0147265.

Jones, R. S. G., Brito da Silva, A., Whittaker, R. G., Woodhall, G. L. and Cunningham, M. O., 2016. Human brain slices for epilepsy research:pitfalls, solutions and future challenges. Journal of Neuroscience Methods, 260, pp. 221-232.

Prokic, E. J., Weston, C., Yamawaki, N., Hall, S. D., Jones, R. S. G., Stanford, I. M., Ladds, G. and Woodhall, G. L., 2015. Cortical oscillatory dynamics and benzodiazepine-site modulation of tonic inhibition in fast spiking interneurons. Neuropharmacology, 95, pp. 192-205.

Lench, A., Robson, E. and Jones, R., 2015. Differential effects of D-cycloserine and ACBC at NMDA receptors in the rat entorhinal cortex are related to efficacy at the co-agonist binding site. PLoS ONE, 10 (7), e0133548.

Prokic, E., Weston, C., Yamawaki, N., Hall, S., Jones, R., Stanford, I., Ladds, G. and Woodhall, G., 2015. Benzodiazepine-site modulation of tonic inhibition in fast spiking interneurons alters cortical oscillatory dynamics. Neuropharmacology, 95, pp. 192-205.

Lench, A., Massey, P. V., Pollegioni, L., Woodhall, G. and Jones, R., 2014. Astroglial D-serine is the endogenous co-agonist at the presynaptic NMDA receptor in rat entorhinal cortex. Neuropharmacology, 83, pp. 118-127.

Greenhill, S. D., Chamberlain, S. E. L., Lench, A. M., Massey, P. V., Yuill, K. H., Woodhall, G. L. and Jones, R. S. G., 2014. Background synaptic activity in rat entorhinal cortex shows a progressively greater dominance of inhibition over excitation from deep to superficial layers. PLoS ONE, 9 (1), pp. 1-16.

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.

This list was generated on Tue Sep 26 06:10:48 2017 IST.

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