Centre for Discovery Brain Sciences
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Dr Michael Daw

Our research focusses on how synaptic function and plasticity in neonatal animals act to coordinate the development of mature cortical circuitry.

Dr Michael Daw


  • Hugh Robson Building
  • 15 George Square
  • Edinburgh EH8 9XD

Contact details

Personal profile

  • 2015 - present: Edinburgh-Zhejiang lecturer, University of Edinburgh.
  • 2010 - 2015: 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 Theme


Our research focusses on how synaptic function and plasticity in neonatal animals act to coordinate the development of mature cortical circuitry. We are interested in how experience influences this development and how development is altered in neurodevelopmental disorders. Mutations in genes encoding synaptic proteins have been identified in a wide range of neurodevelopmental disorders. Understanding how these mutations affect synaptic function and the implications of this for cortical development is crucial to developing treatments for these conditions.

We study these processes using in vitro electrophysiology, 2-photon imaging and histology currently in 3 main projects.

1. Cortical development in a model of intellectual disabilities: SAP102 knockout mice.

SAP102 is a synaptic protein which binds to NMDA receptors and is required for the synaptic localisation of NMDA and AMPA receptors. Mutations in the gene encoding SAP102 have been identified in patients with X-linked intellectual disabilities. We are studying how loss of SAP102 affects synaptic function and cortical connectivity.

SAP102 is also expressed at excitatory synapses in inhibitory interneurons. We are studying if loss of SAP102 affects the experience-dependent recruitment of these interneurons to form functional inhibitory microcircuits.

2. Pre-seizure development in absence epilepsy.

A point mutation in GABAA receptor γ2 subunits (R43Q) identified in absence epilepsy also causes absence seizures in mice from the 4th postnatal week. Although the R43Q mutation reduces overall inhibition this is not the only mechanism resulting in seizures as presence of the wild-type allele during pre-seizure development is partially protective.

We are studying how development is altered during early postnatal development in these mice. Absence epilepsy patients often also suffer cognitive problems so we compare development in these mice with that in models of cognitive problems (such as SAP102 knockout) not normally associated with seizures.

3. Pharmacological manipulation of specific inhibitory interneuron populations.

Alterations in cortical inhibitory synaptic function have been implicated in many psychiatric disorders including schizophrenia and autism. Cortical inhibition is mediated by GABAergic interneurons which are highly diverse in anatomy and function. Most attempts to alter inhibitory circuits in disease are generalized across all interneurons classes but many studies suggest that individual classes are differentially affected by disease.  We are attempting to find pharmacological approaches to enhance the activity of specific classes of interneuron with the aim of creating alternative therapeutic strategies.


Medical Research Council

Team members



Currie, S.P., Luz, L.L., Booker, S.A., Wyllie, D.J., Kind, P.C., and Daw, M.I. (2017). Reduced local input to fast-spiking interneurons in the somatosensory cortex in the GABAA gamma2 R43Q mouse model of absence epilepsy. Epilepsia. 

Luz, L.L., Currie, S.P., and Daw, M.I. (2017). Alterations in the properties of neonatal thalamocortical synapses with time in in vitro slices. PLoS One 12, e0171897.

Crocker-Buque, A., Currie, S.P., Luz, L.L., Grant, S.G., Duffy, K.R., Kind, P.C., and Daw, M.I. (2016). Altered thalamocortical development in the SAP102 knockout model of intellectual disability. Human molecular genetics 25, 4052-4061.

Crocker-Buque, A., Brown, S.M., Kind, P.C., Isaac, J.T., and Daw, M.I. (2015). Experience-Dependent, Layer-Specific Development of Divergent Thalamocortical Connectivity. Cereb Cortex 25, 2255-2266.

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.