Conjoint Senior Principal Scientist, NeuRA
Professor of Brain Sciences, UNSW
Director (Medicine) EPICentre, UNSW
Director (Research) NeuRA Imaging
Honorary Associate, Macquarie Centre for Cognitive Science, Macquarie University, Sydney
School of Medical Sciences, UNSW
+612 9399 1211
Prof Caroline Rae is a biochemist with a background in magnetic resonance and interdisciplinary brain research. She graduated with a PhD in biochemistry and NMR from The University of Sydney in 1993 and spent four years in Oxford, UK, as a Nuffield Medical Fellow where she pioneered the use of magnetic resonance spectroscopy as a tool in cognitive brain research. In 2005 she was appointed to UNSW as a NewSouth Global Professor, one of only a handful of NHMRC R Douglas Wright Fellows subsequently appointed to chairs. She is currently director of the UNSW Node of the National Imaging Facility and holds a cross-disciplinary (STEAM) appointment in medical data visualisation as a Director of the UNSW Expanded Perception and Interaction Centre (EPICentre).
DR MARK SCHIRA
Honorary Senior Research Officer
: +612 9399 1131
DR SYLVIA GUSTIN Senior Research Officer
ZOEY ISHERWOOD PhD student
BEN ROWLANDS PhD student
Abnormal substantia nigra morphology in healthy individuals, viewed with transcranial ultrasound, is a significant risk factor for Parkinson's disease. However, little is known about the functional consequences of this abnormality (termed 'hyperechogenicity') on movement. The aim of the current study was to investigate hand function in healthy older adults with (SN+) and without (SN-) substantia nigra hyperechogenicity during object manipulation. We hypothesised that SN+ subjects would exhibit increased grip force and a slower rate of force application compared to SN- subjects. Twenty-six healthy older adults (8 SN+ aged 58 ± 8 years, 18 SN- aged 57 ± 6 years) were asked to grip and lift a light-weight object with the dominant hand. Horizontal grip force, vertical lift force, acceleration, and first dorsal interosseus EMG were recorded during three trials. During the first trial, SN+ subjects exhibited a longer period between grip onset and lift onset (i.e. preload duration; 0.27 ± 0.25 s) than SN- subjects (0.13 ± 0.08 s; P = 0.046). They also exerted a greater downward force prior to lift off (-0.54 ± 0.42 N vs. -0.21 ± 0.12 N; P = 0.005) and used a greater grip force to lift the object (19.5 ± 7.0 N vs. 14.0 ± 4.3 N; P = 0.022) than SN- subjects. No between group differences were observed in subsequent trials. SN+ subjects exhibit impaired planning for manipulation of new objects. SN+ individuals over-estimate the grip force required, despite a longer contact period prior to lifting the object. The pattern of impairment observed in SN+ subjects shares similarities with de novo Parkinson's disease patients.
We develop a new approach to functional brain connectivity analysis, which deals with four fundamental aspects of connectivity not previously jointly treated. These are: temporal correlation, spurious spatial correlation, sparsity, and network construction using trajectory (as opposed to marginal) Mutual Information. We call the new method Sparse Conditional Trajectory Mutual Information (SCoTMI). We demonstrate SCoTMI on simulated and real fMRI data, showing that SCoTMI gives more accurate and more repeatable detection of network links than competing network estimation methods.
The inhibitory neurotransmitter γ-aminobutyric acid (GABA) acts through various types of receptors in the central nervous system. GABAρ receptors, defined by their characteristic pharmacology and presence of ρ subunits in the channel structure, are poorly understood and their role in the cortex is ill-defined. Here, we used a targeted pharmacological, NMR-based functional metabolomic approach in Guinea pig brain cortical tissue slices to identify a distinct role for these receptors. We compared metabolic fingerprints generated by a range of ligands active at GABAρ and included these in a principal components analysis with a library of other metabolic fingerprints obtained using ligands active at GABAA and GABAB, with inhibitors of GABA uptake and with compounds acting to inhibit enzymes active in the GABAergic system. This enabled us to generate a metabolic "footprint" of the GABAergic system which revealed classes of metabolic activity associated with GABAρ which are distinct from other GABA receptors. Antagonised GABAρ produce large metabolic effects at extrasynaptic sites suggesting they may be involved in tonic inhibition.