Tuesday, 20 October 2015

Upcoming visitors to SCAN series

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.