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Dr Adam Errington

Hodge Foundation Research Fellow, Neuroscience & Mental Health Research Institute

School of Medicine

Email:
erringtonac@cardiff.ac.uk
Telephone:
+44 (0)29 2068 8343
Location:
3.40, Hadyn Ellis Building, Maindy Road, Cardiff, CF24 4HQ

My lab is interested in dendritic function, the function of corticothalamocortical circuits and their role in neurodevelopmental and neuropsychiartic diseases. Please visit my lab blog for more details:

blog.cardff.ac.uk/acerringtonlab

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Function of cortico-thalamocortical circuits

Most incoming sensory information (with the noted exception of the olfactory system) passes through the thalamus where it is transmitted to the cortex and integrated by complex circuits into our perception of the external world. For many years, it was believed that the thalamus operated as a simple ‘relay’ that passed signals on to higher cortical networks with little, if any, functional processing of information. It is now clear that this assumption is grossly inaccurate and that thalamocortical circuits are intimately involved in information processing, critical brain rhythms and several disease states including epilepsy and schizophrenia (see Saalman and Kastner, 2011, Neuron 71(2): 209-223; Briggs and Usrey, 2011, J Physiol 589.1: 33-40). Cortico-thalamamocortical circuits (see above) are extremely complex and although the majority of sensory processing is performed by cortical circuits, thalamic circuits involving glutamatergic thalamocortical neurons, local circuit interneurons and GABAergic neurons of the thalamic reticular nucleus (TRN) have key functions. It is increasingly recognised that, because of the strong bidirectional connectivity between them, the thalamus and cortex cannot be considered in isolation but should but thought of as two parts of the same dynamically updating circuit that have powerful influences on each other. Our research focuses on the intrinsic and dendritic integrative properties of key neurons within these circuits and the role that corticothalamic projections to thalamic nuclei play in modulating sensory information flow through thalamic microcircuits.

Dendritic Function in Neuropsychiatric Diseases.

A number of human genetic variations that confer high risk for developing neurodevelopmental disorders such as schizophrenia and autism spectrum disorder have been identified by genome-wide association studies (GWAS) in recent years. In particular, changes to large sections of DNA, known as copy number variations (CNVs), that result in insufficient or excessive numbers of copies of certain genes have been strongly linked to severe disease phenotypes. Many CNVs contain genes that have been identified to code for proteins that are highly involved in cellular excitability, in particular a number of key synaptic targets. Furthermore, a number of disease associated genetic changes (e.g. DISC-1, NRG-1, Dysbindin, Cyfip-1) have been strongly linked to pronounced changes in dendritic structure of cortical and hippocampal pyramidal neurons including changes in dendritic length, the number of dendritic branches and differences in the type, density and distribution of dendritic spines. Abnormalities in dendritic structure and in dendritic spines have long been recognised as critical hallmarks of a number of neurodevelopmental disorders. Using a range of models our research focuses on how specific genetic changes contribute to changes in dendritic structure, function and synaptic integration and how this might contribute to disruption of normal brain circuit function in neuropsychiatric diseases.