51cg

Biography

I studied biomedical sciences at the 51cg before completing a PhD at the University of Bristol. Following this, I moved to the University of Edinburgh to work in the lab of Prof. Matt Nolan where I studied the cellular and circuit properties that underlie spatial navigation and learned behaviours. I was appointed as a lecturer at the 51cg in September 2022.

My research focuses on trying to understand changes in the brain in autistic spectrum disorder (ASD). Specifically, I want to investigate whether the large number of genes linked to ASD converge on common pathways and pathologies. My lab will do this using a combination of ex-vivo electrophysiology and advanced microscopy techniques, to test for convergence in physiological and/or morphological changes in neurons across several monogenic ASD models. Following on from this I will then aim to determine whether there are critical periods during which these changes can be reversed. This will increase our understanding of how ASD-related genes regulate neuronal function and potentially allow for the development of interventions and treatments for ASD patients.

Research Overview

A large number of genes are associated with autism spectrum disorders (ASDs), yet little is known as to whether there is a convergence of these genes to a smaller number of phenotypic neuropathologies. My lab aims to develop a new model system to study ASDs, using neurons of the inferior olive (IO). IO neurons express the majority of ASD genes, are a 99.9% homogenous population, have elaborate dendritic spines, and easily quantifiable postsynaptic responses to afferent input. Initial experiments suggest that IO neurons display convergent phenotypes across three ASD models: Fmr1^-/y, Syngap1^+/- and  Nlgn3^-/y.

My lab aims to elucidate the mechanisms underlying convergent ASD phenotypes in IO, with the aim of subsequently reversing the changes observed in ASD models. To address this my lab will combine optogenetic approaches and advanced imaging methods to 1) Determine whether the increase in excitability in IO across ASD models is due to a functional change in ion channels or signalling pathways. 2) Determine if there are morphological changes at the level of the spine using super-resolution microscopy. 3) Determine the molecular mechanisms underlying the changes observed. 4) Determine whether ID/ASD phenotypes in IO can be reversed using pharmacological or viral knock-in or knock-down approaches. 5) Determine if there is a critical period during which ID/ASD model pathologies can be reversed.

Through these objectives, my lab will seek to determine whether there are convergent phenotypes across ASD models and whether there are critical periods during which these can be reversed. This will increase our understanding of how ASD-related genes regulate neuronal function and potentially allow for the development of interventions and treatments for ASD patients.

Teaching Responsibilities

Developmental Neuroscience (with Anatomy) - AN4301

Developmental Neuroscience - PY4302

Neuroscience and Neuropharmacology - BM3502

Neuroscience Research Topics - BM3804