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Dr Sue Jones

Dr Sue Jones

University Senior Lecturer


Office Phone: +44 (0) 1223 333795

Biography:

Sue's love of ion channels and their modulation started during her degree in Pharmacology at King's College London and continued during her PhD in the lab of Professor David Brown at University College London, where she identified G proteins involved in the modulation of M-type K+ currents. She moved from voltage gated ion channels to ligand gated ion channels during her postdoctoral work, first with Dr Jerry Yakel at NIEHS, where she studied nicotinic AChRs and 5HT3Rs, and then with Dr Julie Kauer at Duke University, where she studied modulation and plasticity at excitatory synapses. Since moving to Cambridge in 2001 she has focussed on the properties and modulation of glutamate receptors, particularly the NMDA receptor.

Research Interests

NMDA receptors and synaptic control of dopamine neurons in the substantia nigra pars compacta

Substantia nigra dopamine neurons form part of the basal ganglia circuit, which is needed for motivated voluntary movement control. Degeneration of dopamine neurons is a characteristic feature of Parkinson’s disease. We study glutamatergic synapses onto dopamine neurons, with a particular interest in NMDA glutamate receptors: how they are regulated, and the balance between physiological and pathological NMDA receptor activity. This work has been funded by the BBSRC, Parkinson’s UK, the Wellcome Trust and the Isaac Newton Trust.

Teaching

Part II Modules P1, N2, N9

Part IB NST Neurobiology and MVST Neurobiology of Human Behaviour

Part IA MVST Functional Architecture of the Body

Key Publications

Morris PG, Mishina M, Jones S (2018), Altered synaptic and extrasynaptic NMDA receptor properties in substantia nigra dopaminergic neurons from mice lacking the GluN2D subunit, Frontiers in Cellular Neuroscience, In Press                 

Zhao J, Baudry M, Jones S (2018), Calpain inhibition reduces NMDA receptor rundown in rat substantia nigra dopamine neurons, Neuropharmacology, 137:221-229 https://www.ncbi.nlm.nih.gov/pubmed/?term=Zhao+Baudry+Jones

Wild AR, Bollands M, Morris PG, Jones S, (2015), Mechanisms regulating spill-over of synaptic glutamate to extrasynaptic NMDA receptors in mouse substantia nigra dopaminergic neurons, European Journal of Neuroscience, 42:2633-2643

Wild AR, Jones S, Gibb AJ, (2014), Activity dependent regulation of NMDA receptors in substantia nigra dopaminergic neurones, J Physiology, 592.4:653–668

Wild AR, Akyol E, Brothwell SLC, Kimkool P, Skepper JN, Gibb AJ, Jones S, (2013), Memantine block depends on agonist presentation at the NMDA receptor in substantia nigra pars compacta dopamine neurones, Neuropharmacology, 73:138-146

Brothwell SLC , Barber JL, Monaghan DT, Jane DE, Gibb AJ, Jones S, (2008), NR2B- and NR2D-containing synaptic NMDA receptors in developing rat substantia nigra pars compacta dopaminergic neurones, J Physiology, 586:739-750

Plain English

Neurons are the cells in your brain that use electrical and chemical signals to communicate with each other. We study a particular type of brain neuron, the dopamine neuron, which uses the chemical dopamine to control your voluntary movement. Dopamine neurons are lost in Parkinson’s disease. We are particularly interested in a membrane protein, the NMDA glutamate receptor, which is activated by another chemical signal, glutamate, and is very important for regulating  plasticity and memory and the brain. We study the properties of NMDA glutamate receptors in dopamine neurons.

Dopamine neurons in the substantia nigra have been immunolabelled with an antibody (red) and a nuclear stain (blue) to enable us to determine the density of dopamine neurons under different conditions. NMDA reduces the density, and this effect is reversed by memantine. From Wild et al., 2013.

Above: Dopamine neurons in the substantia nigra have been immunolabelled with an antibody (red) and a nuclear stain (blue) to enable us to determine the density of dopamine neurons under different conditions. NMDA reduces the density, and this effect is reversed by memantine. From Wild et al., 2013.

The use-dependent NMDA receptor antagonist, memantine reduces NMDA receptor mediated synaptic currents in response to high frequency stimulation, but not those in response to low frequency stimulation. From Wild et al., 2013.

Above: The use-dependent NMDA receptor antagonist, memantine reduces NMDA receptor mediated synaptic currents in response to high frequency stimulation, but not those in response to low frequency stimulation. From Wild et al., 2013.

Above: NMDA receptors at excitatory synapses in dopamine neurons are composed of GluN2B (ifenprodil-sensitive) and GluN2D (UBP141-sensitive) subunits. From Brothwell et al., 2008.