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Colin J. Akerman
Researcher at University of Oxford
Publications - 68
Citations - 4548
Colin J. Akerman is an academic researcher from University of Oxford. The author has contributed to research in topics: Biology & GABAA receptor. The author has an hindex of 28, co-authored 58 publications receiving 3489 citations. Previous affiliations of Colin J. Akerman include Cold Spring Harbor Laboratory.
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Random synaptic feedback weights support error backpropagation for deep learning.
TL;DR: A surprisingly simple mechanism that assigns blame by multiplying errors by even random synaptic weights is presented, which can transmit teaching signals across multiple layers of neurons and performs as effectively as backpropagation on a variety of tasks.
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Backpropagation and the brain
Timothy P. Lillicrap,Adam Santoro,Luke Marris,Colin J. Akerman,Geoffrey E. Hinton,Geoffrey E. Hinton +5 more
TL;DR: It is argued that the key principles underlying backprop may indeed have a role in brain function and induce neural activities whose differences can be used to locally approximate these signals and hence drive effective learning in deep networks in the brain.
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The X-linked mental retardation protein oligophrenin-1 is required for dendritic spine morphogenesis.
Eve-Ellen Govek,Eve-Ellen Govek,Sarah E. Newey,Colin J. Akerman,Justin R. Cross,Lieven Van der Veken,Linda Van Aelst,Linda Van Aelst +7 more
TL;DR: It is reported that oligophrenin-1, a Rho-GTPase activating protein that is absent in a family affected with MRX, is required for dendritic spine morphogenesis and an interaction between oligophreitol-1 and the postsynaptic adaptor protein Homer is demonstrated.
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Control of axon branch dynamics by correlated activity in vivo.
TL;DR: A correlation-based mechanism by which visual experience directly governs axon branch dynamics that contribute to the development of topographic maps is described.
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Optogenetic silencing strategies differ in their effects on inhibitory synaptic transmission.
TL;DR: Using rodent hippocampal neurons, it is found that silencing activity with a chloride pump can increase the probability of synaptically evoked spiking after photoactivation; this did not occur with a proton pump.