Akerman, Colin - University of Oxford - Department of Pharmacology

个人简介

Dr Akerman joined the Department from Cold Spring Harbor Laboratory, New York. While there, he used a combination of electrophysiological, molecular and optical techniques to investigate how glutamatergic and GABAergic synaptic transmission interact during neural circuit formation and plasticity. This multidisciplinary approach underpins the work in Dr Akerman’s own lab. He conducted his doctoral studies in the Department of Physiology, Oxford, where he worked with Professor Ian Thompson on the role of early synaptic activity in the development of the mammalian thalamus and cortex. Following the completion of his PhD in 2001, Dr Akerman was awarded a Wellcome Trust Travelling Fellowship which he held in the laboratory of Professor Holly Cline. In 2005 he returned to Oxford and was selected to hold a RCUK Fellowship. He started his own lab in 2007 and was appointed as a University Lecturer in 2010.

研究领域

Dr Akerman’s group is examining the principles underlying synaptic circuit formation and plasticity. The group’s work combines electrophysiological assessment of synaptic transmission, single and multi-photon confocal imaging of neurons, and molecular-genetic techniques to both observe and manipulate synaptic circuit development and plasticity. The group is exploring three areas: How do neurons select their synaptic partners? How are synaptic circuits affected by activity-dependent processes? How do neurons integrate excitatory and inhibitory synaptic inputs? The type, strength, and distribution of synaptic connections determine the behavior of individual neurons within a neural network. For instance, experimental and computational modeling data demonstrate that the pattern of excitatory (glutamatergic) and inhibitory (GABAergic) synaptic inputs across the dendritic tree dictates how information is integrated and stored. 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 Dr Akerman’s group. For example, the group is interested in establishing how the connectivity of an individual neuron becomes restricted during its development. But equally, how do activity-dependent processes enable a neuron to adjust the weights of its synaptic connections in the appropriate way? This is particularly relevant during development, when the external environment is known to shape neuronal response properties and mechanisms that control synaptic strength are sensitive to the spatiotemporal patterns of neural activity. A related question is how neurons establish and maintain the correct arrangement of excitatory and inhibitory synaptic inputs. The major inhibitory neurotransmitter in the mature brain is GABA. During development however, and interestingly also in epilepsy, GABA can exert excitatory effects. This results from changes in intracellular chloride, which alters the driving force on chloride permeable GABAA receptors. Dr Akerman’s group are examining how such a fundamental shift in GABAergic signaling influences ongoing network activity and activity-dependent processes.

近期论文

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van Rheede, JJ, Richards, BA, and Akerman, CJ (2015) Sensory-Evoked Spiking Behavior Emerges via an Experience-Dependent Plasticity Mechanism. Muldal, AM, Lillicrap, TP, Richards, BA, and Akerman, CJ (2014) Clonal relationships impact neuronal tuning within a phylogenetically ancient vertebrate brain structure. Ellender, TJ, Raimondo, JV, Irkle, A, Lamsa, KP, and Akerman, CJ (2014) Excitatory effects of parvalbumin-expressing interneurons maintain hippocampal epileptiform activity via synchronous afterdischarges. Herrgen, L, Voss, OP, and Akerman, CJ (2014) Calcium-dependent neuroepithelial contractions expel damaged cells from the developing brain. Raimondo, JV, Joyce, B, Kay, L, Schlagheck, T, Newey, SE, Srinivas, S, and Akerman, CJ (2013) A genetically-encoded chloride and pH sensor for dissociating ion dynamics in the nervous system. Raimondo, JV, Kay, L, Ellender, TJ, and Akerman, CJ (2012) Optogenetic silencing strategies differ in their effects on inhibitory synaptic transmission. Raimondo, JV, Markram, H, and Akerman, CJ (2012) Short-term ionic plasticity at GABAergic synapses. Ilie, A, Raimondo, JV, and Akerman, CJ (2012) Adenosine release during seizures attenuates GABAA receptor-mediated depolarization.