Dates for your diaries
The Sensory Cognitive and Affective Neuroscience
(SCAN) research group is hosting three visiting speakers in the next few weeks.
Please join us for the talks! Each speaker has a brief stay in Newcastle but if
you would like to meet with them let me know (Juanita.Todd@newcastle.edu.au)
and I might be able to arrange it for you.
Date: Wednesday October 21st 12-1pm
Venue &
Time: Keats Reading Room, Callaghan Campus (VC connection
to Science Offices Ourimbah)
Speaker: Dr
Jacqueline Rushby
Postdoctoral
Fellow, UNSW
TOPIC: Diminished Arousal and Emotional
Responsivity after Severe Traumatic Brain Injury.
Severe traumatic brain injury (TBI) results from
acceleration-deceleration forces (often sustained in motor vehicle accidents,
falls and assault) and leads to heterogeneous effects on the brain, with a
preponderance of multifocal damage to the lateral, anterior and ventral
surfaces of the frontal and temporal lobes, and diffuse axonal damage. In addition
to cognitive impairment, TBI is often characterised by emotional changes, poor
behavioural regulation, inattention and poor social function. Around two
thirds of patients with TBI experience deficits in arousal and emotional
responsivity. Firstly I will present evidence from several studies showing
impairments are manifested both physiologically and behaviourally, and that
this basic deficit in arousal, manifests as an inability to mobilise arousal
for normal everyday function. The discovery of the mirror neuron system (MNS)
in the human brain has provided a neurobiological substrate for understanding
human social cognition directly relevant to the emotional processing deficits
observed in TBI. While a large body of research has investigated MNS function
in Autism Spectrum Disorder (ASD), there have been no studies investigating MNS
functioning in individuals with TBI. However, this group represents an
important opportunity to examine MNS function in a population with an acquired
social cognition deficit, in contrast to the developmental deficit found in
ASD. In this talk, I will describe how
disrupted neural networks, specifically focusing upon EEG indices of functional
connectivity, may explain mu suppression deficits in TBI. Possible
treatments to repair MNS function will be proposed.
Date: Wednesday November 4th 12-1pm
Venue &
Time: Keats Reading Room, Callaghan Campus (VC connection
to Humanities Offices in Ourimbah)
Speaker: Dr
Thomas Whitford
Senior
Lecturer and NHMRC Career Development Fellow, UNSW
TOPIC: Self-suppression and schizophrenia (or why
you can’t tickle yourself, and why it matters)
Self-generated
sensations typically feel less salient than externally-generated sensations –
the fact that it is difficult to tickle oneself is a well-known example.
Consistent with this phenomenon, self-generated sensations, such as the sound
of one’s own voice, normally evoke less activity in the electroencephalogram
(EEG) than physically identical, externally-produced sensations. There is
evidence to suggest that people with schizophrenia do not exhibit this
‘electrophysiological self-suppression’, which may account for their
characteristic tendency to misattribute self-generated thoughts and actions to
external agents. This presentation will review the evidence for
‘electrophysiological self-suppression’ deficits in schizophrenia and discuss
the potential utility of ESS deficits as a biomarker for psychosis-proneness.
Date: Wednesday November 11th 12-1pm
Venue &
Time: Keats Reading Room, Callaghan Campus (VC connection
to Science Offices Ourimbah)
Speaker: Associate
Professor Thomas Burne
Conjoint Principle
Research Fellow, QBI
TOPIC: Translational neuroscience; from
epidemiology to animal models
There are many environmental risk factors that impact
on brain development and behaviour of relevance to neuropsychiatric disorders,
such as autism and schizophrenia. However, selecting the appropriate candidate,
the right animal model and the most informative outcome is a challenging task.
We have embarked on a program of research focusing on translational
neuroscience, to model candidate risk factors in animal models relevant to
neurodevelopmental disorders. We have been investigating modifiable risk
factors, including vitamin D deficiency, stress, alcohol exposure and advanced
paternal age. We typically use a standard battery of behavioural tests to asses
a range of behavioural domains, as well as structural and neuroanatomical
outcomes. The animal models we have generated produce variable and subtle
behavioural and structural phenotypes. The relevance of each particular animal
model to a particular disorder is not always obvious, because the models
ultimately inform us about the impact of a single variable on brain development
and behaviour in a rodent, and this may have broader implications for brain
function in humans, rather than be informative for a specific disorder.
Ultimately, convergent evidence from different animal models will offer the
most promise in unravelling the delicate interaction between genotype and
environment on brain development and behaviour.
