Centre for Genomic & Experimental Medicine
Centre for Genomic & Experimental Medicine

Peter Kind (Affiliate)

Examining cellular and circuit dysfunction associated with monogenic forms of autism and intellectual disability.

Photo of Professor Peter Kind
Professor Peter Kind

Research in a Nutshell

The Kind laboratory examines how cellular and circuit dysfunction leads to altered behaviour in models of autism and intellectual disability. Our research is designed to address two key questions:

 1. Do developmental disorders have critical periods for treatment?

For decades it was believed that the adult brain was hard-wired, and that interventions for autism would be most effective if implemented during the first few years of life. This dogma has recently been questioned for several monogenic forms of autism with intellectual disability. To determine whether there are critical periods for therapeutic intervention, we employ proof-of-concept genetic and pharmaceutical rescue studies to determine the effectiveness of potential therapies.

By employing a systematic approach to reversibility, as well as identifying developmental trajectories for the appearance of cellular, circuit and cognitive deficits, we address fundamental questions about the extent to which autism can be treated throughout the lifespan.

 2. Does genetic heterogeneity mask underlying convergence onto a common developmental pathophysiology?  

Of the many genes that have been causally-linked to autism, many cluster around common cellular processes including synaptic function and epigenetic regulation. This genetic convergence raises the possibility of common therapeutic avenues for diverse genetic causes. We examine whether different genetic models of autism display recurrent cellular, circuit and/or behavioural phenotypes that respond to common treatment strategies.

Our recent studies suggest many of the cellular phenotypes observed in our models reflect homeostatic or compensatory changes in neuronal function. These compensatory changes serve to lessen the cellular and circuit effects of genetic mutations and could explain, in part, apparent physiological and behavioural convergence between models.



Peter Kind

Professor of Developmental Neuroscience

Owen Dando Postdoctoral Fellow

Anjanette Harris

Postdoctoral Fellow
Emma Perkins Postdoctoral Fellow

Xin He

Postdoctoral Fellow
Felicity Inkpen Postdoctoral Fellow

Jorge Maicas Royo

Postdoctoral Fellow
Sally Till Postdoctoral Fellow

Anna Toft

Postdoctoral Fellow

Thomas Watson

Postdoctoral Fellow
Darren Walsh Postdoctoral Fellow

Kosala Dissanayake

Postdoctoral Fellow
Raven Hickson PhD Student
Mary O'Keeffe PhD Student
Vanesa Salazar Sanchez PhD Student
Jingjing Ye PhD Student

Mahdie Ezabadi

PhD Student

Lynsey Dunsmore

Technical Manager

Karen Biggar


Jane Wright

SIDB Centre Administrator

Nicole Cuthbert

Research Technichian

Dan Giffney

Research Technichian

Chloe Henley

Research Technichian

Will Farnworth-Rowson

Research Technichian

Brittany Prokop

Research Technichian
Jess Rodda Research Technichian




  • Mark Bear, Picower Centre, MIT, Cambridge, USA
  • Matt Jones, University of Bristol
  • Frank Sengpiel, University of Cardiff
  • Robert Datta, Harvard University
  • Siddharthan Chandran, University of Edinburgh
  • Sumantra Chattarji, University of Edinburgh
  • Giles Hardingham, University of Edinburgh
  • Emily Osterweil, University of Edinburgh
  • Nathalie Rochefort, University of Edinburgh
  • David Wyllie, University of Edinburgh
  • Emma Wood, University of Edinburgh
  • Sam Booker, University of Edinburgh
  • Adrian Bird, University of Edinburgh
  • Oliver Hardt, University of Edinburgh
  • Alfredo Gonzalez-Sulser, University of Edinburgh
  • Stuart Cobb, University of Edinburgh


Scientific Themes

Neurodevelopmental disorders, autism, intellectual disability, behaviour, cellular and circuit electrophysiology, rats

Technology Expertise

Electrophysiology, imaging, behaviour