More awards for our students!
Florey Neuroscience Institutes Miller Travel Fellowship for 2011
Congratulations to Robert Hatch for being awarded this very competitive travel fellowship!
This will enable Rob to visit Prof Kaila’s Laboratory of Neurobiology, located at the University of Helsinki, Finland. Here he will have the incredible opportunity to learn the art of in vitro pH imaging, which will enhance his already impressive knowledge and skill set.
Ayse Berke and Liana Colvill Travel Award for 2011
Congratulations to Tae Hwan Kim for receiving his THIRD award for the year!
This will give Kim the opportunity to present his impressive research at a national or international conference of his choice.
Well done boys.
Successful grant applications!
The Ion Channels and Diseases Laboratory have been very successful in this year’s funding outcomes.
ARC Discovery Projects for funding commencing in 2012:
Approved Project Title: Genetic dissection of functional-structural connectivity using optogenetic fMRI and dMRI
Tractography
Petrou, A/Prof Steven; Calamante, A/Prof Fernando; Reid, Dr Christopher A
Project Summary
The project will map the connectivity pattern of genetically defined neurons in mouse brain by combining state of the art
molecular and neuroscience imaging technology. The outcome will be a significant step toward building a complete
functional and structural mapping resource, with application for examining dysfunction in neurological disease models.
Approved Project Title: Brain sodium channel: functional role of developmentally regulated alternative splicing
Petrou, A/Prof Steven; Reid, Dr Christopher A
Project Summary
This project will identify the roles of neonatal and adult forms of a sodium channel in the function of neurons in the
developing brain. Sodium channels are vital for brain function and this study will improve our understanding of the
function of healthy brain as well as of underlying mechanisms of some neurological disorders.
NHMRC Project Grant for funding commencing in 2012.
Approved Project Title: Neuroanatomical correlates of susceptibility in a model of genetic epilepsy.
Dr Verena Wimmer
Starting work in the Melbourne Brain Centre!
RELOCATION OF ION CHANNELS AND DISEASES LABORATORY.
The Ion Channels and Diseases laboratory, along with the Howard Florey Institute, moved into the Melbourne Brain Centre in August this year.
The $225 million Melbourne Brain Centre is located in Parkville and is the largest brain research centre in the southern hemisphere. It houses 700 scientists from Florey Neuroscience Institutes, the Mental Health Research Institute and the University of Melbourne to research brain disorders such as stroke, multiple sclerosis, Parkinson’s Disease, Alzheimer’s disease, mental illness and of course – Epilepsy.
Our laboratory quickly settled into this highly collaborative centre with state of the art equipment.
Bryan's award winning presentation!
Congratulations Bryan on your award winning presentation!
2nd place in the Student Brain Symposium 2011
Neurophysiological mechanisms in a mouse model of early onset epileptic encephalopathy
Bryan Leaw, Christopher Reid and Steven Petrou
Howard Florey Institute, Parkville, 3010
Dravet syndrome is a severe epileptic encephalopathy, which lies at the most severe end of the Genetic Epilepsy with Febrile Seizure Plus (GEFS+) spectrum. SCN1A mutations are the most common cause of GEFS+ and account for >70% of patients with Dravet syndrome. Recently however, a patient with Dravet syndrome was reported to be homozygous for a mutation in SCN1B, encoding the β1 subunit of sodium channels. To further elucidate the pathogenesis of SCN1B based Dravet syndrome, we investigated a mouse model homozygous for a common GEFS+ SCN1B mutation, C121W. Mice homozygous for this C121W mutation exhibited the seizure susceptibility and abnormal gait of human Dravet patients, and mirrored human patient responses to specific anti-epileptic drugs (AED). This strongly supported the C121W mouse as a model of Dravet syndrome, therefore we performed neuronal analysis with the presence of the C121W mutation. We examined homozygous subicular neurons, which have been suggested to have a role in thermal seizure genesis. These neurons displayed hallmarks of increased excitability, consisting broader APs and a left-shifted input-output relationship. Interestingly, these neurons displayed intrinsically higher membrane input resistance, which could account for this hyperexcitability. We then tested a novel AED, retigabine, which activates potassium channels and thereby would potentially lower membrane resistance back to wild-type levels. Work done in our laboratory then showed that upon application of retigabine, susceptibility to thermal seizures in these mice was strongly suppressed. This highlights the potential of our mouse model in identifying potential AEDs that could target specific human epileptic syndromes.
 Bryan's Sobr presentation.pdf | [ ] | 989 Kb |
Kim's award winning poster!
Congratulations Kim on your award winning poster!
1st place in the Student Brain Symposium 2011
1st place in the 8th Asian & Oceanian Epilepsy Congress 2010
Low blood glucose precipitates spike-and-wave discharge activities in a mouse model of epilepsy
Tae Hwan Kim1.3, Christopher A. Reid1,3, Samuel F. Berkovic2 and Steve Petrou1,3
1. Florey Neuroscience Institute The University of Melbourne, Parkville, Australia
2. Department of Medicine, Austin Health, The University of Melbourne, Heidelberg West, Australia
3. Centre for Neuroscience, The University of Melbourne, Parkville, Australia
Absence seizures are defined as unprovoked behavioural arrest associated with generalized spike and wave discharge (SWD) on EEGs. Absence epilepsies have a largely genetic aetiology but it is well known that environmental effects such as decreased vigilance and voluntary hyperventilation may induce seizures. However, we still don’t have a complete understanding of all the environmental precipitants. Low glucose in general has not been considered an environmental factor but the manifestation of absence epilepsy in patients with brain glucose transporter deficiencies has raised this possibility. Here we investigate if lowering blood glucose can precipitate SWD activity in a animal model of absence epilepsy.
This study highlights a highly reproducible, immediate, reversible and dose dependent impact of low blood glucose on SWD expression in the animal model of absence epilepsy. We also showed that overnight fasting can reduce blood glucose levels sufficiently to precipitate SWD activity. Our findings suggest that low blood glucose needs to be considered as a potential environmental risk factor in absence epilepsy motivating further clinical studies into this phenomenon.
| Poster (ILAE Congress).pdf | [ ] | 328 Kb |