School of Life Sciences

I initially read Physiology at Cardiff University, where I remained to complete a PhD in neurotransplantation at the Brain Repair Group. After completing my PhD, I spent my first post-doc at Cardiff, working on the regulation of bi-directional striatal synaptic plasticity by CREB; and my second post-doc at Bristol University working on multi-unit recordings in freely moving animals.

I obtained my first academic position at Cardiff University, and later took up lectureships at universities in Australia and Oxford.  In August 2011 I moved, along with my lab, to Keele.

 Understanding how the brain responds to injury is fundamental to the development of new treatments and innovative therapies. My research focuses on the role of the Basal Ganglia (BG) in a range of distinct pathologies and environmental manipulations. The BG is a collection of structures within the mammalian brain traditionally associated with controlling movement. However, it is now quite clearly understood that these structures play a role in a range of cognitive functions such as motor learning, habit formation, working memory, and drug addiction.

My current research can be divided into two main areas:

1. Striatal Grafts

Transplantation of embryonic striatal cells into the BG of patients suffering from Huntington’s (HD) and Parkinson’s disease (PD), producing a striatal graft, is an exciting potential experimental therapeutic, due to it’s ability to replace and repair the damaged host neuronal circuitry.

Using a range of basal ganglia pathology models we assess the efficacy of graft integrations using a range of electrophysiology, histology and behavioral studies.  Ultimately, we aim to demonstrate that embryonic striatal grafts ‘functionally integrate’ with the host neuronal network.  We have previously shown that striatal grafts restore baseline transmission and synaptic plasticity, within models of HD (Mazzocchi-Jones, et al 2005: 2009), and that such plasticity is influenced by environmental manipulation (Mazzocchi-Jones, et al 2011).  We now aim to demonstrate that such ‘functional integration’ displays a direct link between synaptic mechanisms and behavioral recovery.

2. Basal Ganglia Development

Over the last decade a growing body of evidence has suggested that abnormal development of the BG may play a role in a diverse range of neurodevelopmental conditions.  We are specifically interested in elucidating the role of the BG in in two such conditions, namely cerebral palsy, and schizophrenia.

We are currently applying a range of histological, electrophysiology, and molecular biology techniques to our BG development models.  We hope to identify a range of molecular and chemical factors controlling developmental plasticity of the BG, in the hope that such targets may prove suitable for therapeutic intervention.   

Images:

• Top - Medium Spiny Neuron
• Middle - Transplantation of embryonic striatal cells creates a striatal graft. DARPP-32 and AChE are positive indicators of striatal cells.
• Lower - The Graft in vitro brain slice. Transplanted embryonic striatal cells, from a GFP tagged donor, can be identified by their endogenous fluorescence. Host-Graft synaptic physiology is investigated via stimulation of the host cortical fibres, and recording from transplanted striatal neurones.