Dr Michael Daw

Michael Daw
  • Dr Michael Daw
  • Career Development Fellow
  • Hugh Robson Building room 108 15 George Square
  • Edinburgh EH8 9XD
  • Work: +44 (0)131 650 3722
Email:

One of my research interests is the cellular and synaptic events which underlie cortical development.

Personal profile

  • 2010-present: Career Development Fellow, University of Edinburgh
  • 2006-2009: Visiting Fellow, NIH, Bethesda, MD, USA
  • 2002-2006: Research Assistant, University of Bristol
  • 1999-2002: PhD, University of Bristol

Research

The Barrel Cortex Model of Cortical Function and Development

The Barrel Cortex Model of Cortical Function and Development The thalamocortical (TC) input to the rodent barrel cortex is a relay for sensory information from the whiskers.

This information is processed in the cortex to allow the animal to perceive shape, location and even texture of objects contacted by the whiskers.

We take advantage of the unique features of this system to study the cellular and synaptic events which underlie cortical development. Single and double patch-clamp recordings are made from cortical cells in the in vitro TC slice preparation.

We use these recordings to study how the cortex processes sensory input and also to study forms of synaptic plasticity thought to underlie the sensory-dependent development of this system.

In particular we are interested in how network activity affects the induction of synaptic plasticity and how the activity of inhibitory interneurons shapes the sensory input in the cortex.

The cortex contains multiple classes of inhibitory interneuron each serving specialised functions such that identification of recorded interneurons is necessary to fully understand the roles of these cells.

To this end cells are filled with biocytin during whole-cell recordings for subsequent morphological categorisation and mRNA expression profiles are established using single-cell rtPCR.

Cortical Development in Fragile-X-Syndrome

Together with Peter Kind we are using the information gained about normal development and function to identify abnormalities in a model of fragile-X-syndrome (FXS).

FXS is the commonest geneticically-inherited cause of mental retardation and sufferers show impaired development of cognitive abilities associated with cortical processing.

We hope that identifying developmental defects on a cellular level will lead to treatments which will stop the progression of FXS.

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Funding

My work is funded by the Medical Research Council.

Team members

  • Stephen Currie (Post-doc)
  • Max Whittaker (PhD student)

Collaborations

I am collaborating with Prof Peter Kind, University of Edinburgh.

Publications

Crocker-Buque A, Brown SM, Kind PC, Isaac JT, Daw MI. (2014) Experience-Dependent, Layer-Specific Development of Divergent Thalamocortical Connectivity. Cereb Cortex. Mar 7

Daw MI, Pelkey KA, Chittajallu R, McBain CJ (2010) Presynaptic kainate receptor activation preserves asynchronous GABA release despite the reduction in synchronous release from hippocampal cholecystokinin interneurons. Journal of Neuroscience 30:11202-9.

Daw MI, Tricoire L, Erdelyi F, Szabo G, McBain CJ (2009) Asynchronous transmitter release from cholecystokinin-containing inhibitory interneurons is widespread and target-cell independent. Journal of Neuroscience 29:11112-11122.

Daw MI, Ashby MC, Isaac JT (2007) Coordinated developmental recruitment of latent fast spiking interneurons in layer IV barrel cortex. Nature Neuroscience 10:453-461.

Daw MI, Scott HL, Isaac JT (2007) Developmental synaptic plasticity at the thalamocortical input to barrel cortex: mechanisms and roles. Mollecular and Cellular Neuroscience 34:493-502.

Daw M, Isaac J (2007) Electrophysiological recordings from neonatal neocortical brain slices. Current Protocols in Neuroscience Chapter 6:Unit 6 23.

Daw MI, Bannister NV, Isaac JT (2006) Rapid, activity-dependent plasticity in timing precision in neonatal barrel cortex. Journal of Neuroscience 26:4178-4187.

Daw MI, Bortolotto ZA, Saulle E, Zaman S, Collingridge GL, Isaac JT (2002) Phosphatidylinositol 3 kinase regulates synapse specificity of hippocampal long-term depression. Nature Neuroscience 5:835-836.


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