Research summary

Dr Nigel Emptage

We are examining the mechanisms of an activity-dependent form of neural plasticity known as long-term potentiation (LTP). LTP is widely regarded as the synaptic substrate for certain forms of learning and memory. By understanding the details of synaptic transmission following the induction of LTP we aim to gather insight into the processes that underlie memory formation.

Our experimental approach combines high-resolution live cell fluorescent imaging methods with electrophysiology enabling us to monitor neurotransmission at individual synapses. Within the laboratory we have facilities that include multi-photon and confocal microscopes. These are principally used for our single synapse imaging experiments. We also have a high-speed CCD imaging facility that enables us to measure fluorescent signals that arise at regions of the cell not confined within the synapse. Additionally we have a recently developed dual-wavelength total internal reflection microscope (TIRF) for the study of endo- and exocytosis.

Recent work by the group has reported that silent synapses, when unmasked by the induction of LTP, show an exclusively post-synaptic mode of expression whereas potentiation of formerly silent synapses reveals a pre-synaptic expression mechanism (Ward et al. Neuron 2006). We are now attempting to understand the basis of the state-dependence of the synapse.

Dr Emptage joined the Department in 2000 from the National Institute for Medical Research, London. While there he, in collaboration with Dr Tim Bliss, FRS and Professor Alan Fine, developed optical methods for the imaging of synaptic activity in living neural tissue. Dr Emptage is continuing with the strategy of combining electrophysiology and high resolution imaging methods (confocal/multi-photon/TIRF) to examine the integrative actions of the single synapses.

Dr Emptage was a graduate student in the Department of Zoology, Cambridge where he worked with Professor Malcolm Burrows, FRS examining sensory-motor information processing in the locust. Following the completion of his PhD in 1991, Dr Emptage received a SERC-NATO fellowship which he held in the laboratory of Professor Tom Carew at Yale University, USA. It was during this period that he became interested in the cellular mechanisms of synaptic plasticity.

2012

Synaptic bistability due to nucleation and evaporation of receptor clusters.

Burlakov, VM, Emptage, N, Goriely, A, and Bressloff, PC
Phys Rev Lett, 108(2):028101.

Wavelength-orthogonal photolysis of neurotransmitters in vitro.

Stanton-Humphreys, MN, Taylor, RDT, McDougall, C, Hart, ML, Brown, CTA, Emptage, NJ, and Conway, SJ
Chem Commun (Camb), 48(5):657-9.

2011

Imaging synaptic plasticity.

Padamsey, Z and Emptage, NJ
Mol Brain, 4:36.

Increased expression of dysbindin-1A leads to a selective deficit in NMDA receptor signaling in the hippocampus.

Jeans, A, Malins, R, Padamsey, Z, Reinhart, M, and Emptage, N
Neuropharmacology, 61(8):1345-53.

2010

Analysis of microscopic parameters of single-particle trajectories in neurons.

Burlakov, VM, Taylor, R, Koerner, J, and Emptage, N
Biophys J, 99(5):1368-76.

Neuronal low-density lipoprotein receptor-related protein 1 binds and endocytoses prion fibrils via receptor cluster 4.

Jen, A, Parkyn, CJ, Mootoosamy, RC, Ford, MJ, Warley, A, Liu, Q, Bu, G, Baskakov, IV, Moestrup, S, McGuinness, L, Emptage, N, and Morris, RJ
J Cell Sci, 123(Pt 2):246-55.

Presynaptic NMDARs in the hippocampus facilitate transmitter release at theta frequency.

McGuinness, L, Taylor, C, Taylor, RDT, Yau, C, Langenhan, T, Hart, ML, Christian, H, Tynan, PW, Donnelly, P, and Emptage, NJ
Neuron, 68(6):1109-27.