logo
School of Biomedical Sciences
   
   
  
 

Gareth Hathway

Lecturer in Neuroscience, Faculty of Medicine & Health Sciences

Contact

Teaching Summary

I currently convene the Structure, Function and Pharmacology of Excitable Tissues Modules for 1st year Medical students and deliver these lectures to the MPharm first year students as well. I also… read more

Research Summary

My research group is sited within newly refurbished and equipped laboratories within the School of Biomedical Sciences at the University of Nottingham. We are a relatively new but rapidly expanding… read more

Selected Publications

I currently convene the Structure, Function and Pharmacology of Excitable Tissues Modules for 1st year Medical students and deliver these lectures to the MPharm first year students as well. I also contribute significantly to the 3rd year Neuroscience BSc and MSci Honours course module entitled 'Neurobiology of Pain'. I contribute to teaching of practical classes and deliver selected taching on other modules across degree courses. In addition to this I am a tutor on both the Neuroscience and Medical courses.

Current Research

My research group is sited within newly refurbished and equipped laboratories within the School of Biomedical Sciences at the University of Nottingham. We are a relatively new but rapidly expanding lab. I have been successful in attracting funding from the BBSRC and Arthritis Research UK and I am currently recruiting to fill roles on both of these projects. The broad focus of my research is to understand the underlying neurobiological processes that occur when an individual experiences pain. In particular I am interested in the contribution that supraspinal brainstem centres, the rostral ventral medial medulla (RVM) and the periaqueductal grey (PAG) play in the induction and maintenance of chronic pain and also how these centres influence the postnatal maturation of pain processing. These supraspinal sites are central to the action of opioid analgesics, and neurones within these regions are able to powerfully inhibit or facilitate the excitability of neurones within the dorsal horn of the spinal cord and therefore are able to decrease or increase the amount of pain an individual experiences. Alongside my collaborator, Professor Maria Fitzgerald (UCL) I have recently shown that the RVM undergoes profound changes in the postnatal period. Early in life animals and humans have exaggerated responses to pain, pain thresholds are lower, the behavioural responses to painful stimuli are exaggerated and uncoordinated. This increased excitability within the neural pathways that detect and process pain is due to a lack of mature inhibitory neurotransmission in the spinal cord, one source of these inhibitory signals in adults is from the RVM. Early in life the RVM appears to be unable provide inhibitory input to the spinal cord, instead it powerfully facilitates, or excites, pain processing at this level. Our observations have shown that the RVM fully matures at quite a late stage compared to other areas of the CNS and we are in the process of elucidating the mechanisms responsible for this. I also have an on-going collaboration with Dr Suellen Walker (Institute of Child Health, UK) in which we are interested in what the effects of surgical pain in the early postnatal period have upon pain processing throughout the rest of an individual's life. Dr Walker's recent work with children who were born prematurely and required surgery to correct underlying abnormalities has shown that as these children mature they have altered pain thresholds when compared to children who were born prematurely but did not undergo surgery. We are investigating whether this profound alteration in sensory processing can be explained, at least in part, through changes in supraspinal pain processing. Another area of active interest that I am pursuing is trying to understand the interactions between the nervous and immune systems with regard to pain. Alongside colleagues I have demonstrated that the primary immunocompetant cells in the CNS, microglia, can be activated within the spinal cord following physiological stimulation of high-threshold sensory neurones that convey painful information from the periphery to the CNS (C-fibres) in the absence or damage to either the sensory neurones or to the CNS itself. Previously we have known that microglia play an important role in inflammatory and neuropathic pain states, however it wasn't clear if these cells could only be stimulated when neurones were damaged. Microglia and other immune cell types are potential targets for therapeutic intervention in patients suffering from chronic pain. I am pursuing research aimed at understanding how these cells are regulated in areas of the CNS responsible for processing pain and studying their interactions with neurones. In collaboration with the Arthritis Research UK National Pain Centre I am investigating the role of these cells in the establishment of pain associated with osteoarthritis. I use a combination of approaches in my studies including neurophysiological and neurochemical measurements, neuroanatomical studies including immunohistochemistry and neuronal tract tracing, and, in collaboration with colleagues, quantitative assessment of expression levels of neurotransmitters, receptors and other gene products in the CNS (qPCR).

School of Biomedical Sciences

University of Nottingham
Medical School
Queen's Medical Centre
Nottingham, NG7 2UH

telephone: +44 (0) 115 823 0141
email: enquiries