Corpus Christi College Oxford

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Professor Colin Akerman

Colin Akerman

Corange Fellow and Tutor in Physiology, Professor of Neuroscience


I lead a neuroscience research group within the Department of Pharmacology at Oxford University. Our work is focused on understanding general principles by which synaptic connections in the brain are formed and are altered by activity-dependent processes. This is a fundamental challenge if we are to understand how the brain is organised and how it can change in response to information received from the environment. As well as probing these basic mechanisms, the aim is to contribute to a more complete description of how synaptic circuits become altered in conditions such as epilepsy and dementia.

I hold Masters degrees in both Psychology (Edinburgh) and Neuroscience (Oxford) and conducted my doctoral studies in the Department of Physiology at Oxford, where I worked on the role of early synaptic activity during brain development. Following the completion of my DPhil in 2001, I was awarded a Wellcome Trust Fellowship which I held at Cold Spring Harbor Laboratory in New York. While there, I used a combination of molecular, electrophysiological and optical techniques to investigate how early neurotransmission regulates the developing brain. In 2005, I returned to Oxford and was awarded an RCUK Academic Research Fellowship in the Department of Pharmacology, which is where I established my own laboratory in 2008. In the same year, I became the Medical Tutor and Corange Fellow in Physiology at Corpus Christi College.


Evolution has invested heavily in synaptic connections. The human brain, for example, is estimated to contain 0.15 quadrillion synapses, each one taking up approximately 1 cubic micrometre. The type, strength, and distribution of synaptic connections determines the behavior of individual neurons within a neural network. For instance, experimental and computational modeling data demonstrate that the pattern of excitatory and inhibitory synaptic inputs across a neuron’s dendritic tree dictates how information is integrated and stored by the neuron. It is also widely believed that alterations in the formation and/or plasticity of synaptic connections underliedisorders such as epilepsy, schizophrenia and dementia.

These synaptic circuits develop through a combination of ‘hard-wired’ genetic mechanisms and ‘plastic’ activity-dependent processes. Understanding this interplay underlies many of the projects in our group. My research group are interested in establishing how the connectivity of an individual neuron becomes restricted during its development. But equally, how do synaptic plasticity mechanisms enable a neuron to adjust the weights of its connections, such as occur during learning? A related question is how neurons establish and maintain their correct balance of excitatory and inhibitory synaptic inputs. In this regard, we have described novel forms of inhibitory synaptic plasticity, in which local ionic changes can alter the strength of inhibitory synaptic transmission. We have shown that these have important implications during development and in epilepsy.

To study these questions, my group combine electrophysiological assessment of synaptic transmission, single and multi-photon imaging of neural circuits, molecular-genetic manipulation techniques and computational approaches.

Teaching and supervision

I teach at all levels of Oxford's undergraduate course in preclinical Medicine and on graduate courses in Pharmacology and Neuroscience. I tutor Corpus Medical students in their First BM (Years 1-2) and in their Final Honours School (Year 3). My main subject areas include Cellular Physiology, Pharmacology, Neuroscience, Developmental Biology and Molecular Signalling. In addition, I currently coordinate the Neuropharmacology Option in Biochemistry, I'm Examiner for the Masters course in Pharmacology and I am supervising graduate students studying for a DPhil in Neuroscience.

Key Publications

Lillicrap, T.P., Cownden, D., Tweed, DB, Akerman, C.J. (2016) Random synaptic feedback weights support error backpropagation for deep learning. Nature Communications, 7:13276.

van Rheede, J.J., Richards, B.A., Akerman, C.J. (2015) Sensory-Evoked Spiking Behavior Emerges via an Experience-Dependent Plasticity Mechanism.Neuron 87(5):1050-62.

Muldal, A.M., Lillicrap, T.P., Richards, B.A., Akerman, C.J. (2014) Clonal relationships impact neuronal tuning within a phylogenetically ancient vertebrate brain structure. Current Biology 24(16):1929-33.

Ellender, T.J., Raimondo, J.V., Irkle, A., Lamsa, K.P., Akerman C.J. (2014) Excitatory effects of parvalbumin-expressing interneurons maintain hippocampal epileptiform activity via synchronous afterdischarges. Journal of Neuroscience 34(46):15208-22.

Herrgen, L., Voss, O.P., Akerman, C.J. (2014) Calcium-dependent neuroepithelial contractions expel damaged cells from the developing brain. Developmental Cell, 31(5):599-613.

Raimondo, J.V. Kay, L., Ellender, T.& Akerman, C.J. (2012) Optogenetic silencing strategies differ in their effects on inhibitory synaptic transmission. Nature Neuroscience, 15:1102-4.

Richards, B. A., Voss, O.P. & Akerman, C.J. (2010) GABA circuits control stimulus-instructed receptive field development in the tectum. Nature Neuroscience, 13:1098-106.


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