Event Details

Wednesday, 17 October 2018 - Wednesday, 17 October 2018
11:00 am - 12:00 pm
QBI Level 7 Auditorium
UQ Location:
Queensland Brain Institute (St Lucia)
Event category(s):

Event Contact

Ms Deirdre Wilson
3346 6300
Org. Unit:
Queensland Brain Institute

Event Description

Full Description:
Professor Darryl Eyles, Queensland Brain Institute, University of Queensland

Title: “The troubled journey of a dopamine neuron towards psychosis”

The idea that there is some sort of abnormality in dopamine signalling is one of the more enduring hypotheses in schizophrenia research. Opinion leaders produce perspectives on the etiology of this disorder with provocative titles such as ‘Risk factors for schizophrenia—all roads lead to dopamine’ or ‘The dopamine hypothesis of schizophrenia—the final common pathway’. Perhaps, the other most enduring idea about schizophrenia is that it is a neurodevelopmental disorder with a weight of epidemiological research indicating schizophrenia-risk is associated with a wide array of adverse developmental environments such as maternal exposure to infectious agents, toxins, dietary deficiencies or excessive hypoxia from birth complications.

My laboratory (and many others) have modeled developmental risk-factor epidemiology in animals in an attempt to understand how this may produce abnormal brain function. Such studies typically show that adverse “exposure X” leads to behavioural, neurochemical and anatomical abnormalities of relevance to the diverse symptom clusters in schizophrenia. Many of these findings would also appear to be consistent with abnormal dopamine signalling. The burning question remains how can in utero exposure to a specific (developmental) insult induce persistent abnormalities in dopamine signalling in the adult?
The work from my laboratory and that of collaborating groups is now beginning to provide an answer. We consistently show that crucial early processes in the specification and differentiation of dopamine neurons are selectively vulnerable to such adverse environments. This leads to an alteration in the trajectory or “journey” of these neurons towards psychosis-relevant phenotypes.

In the 1st part of this talk I will summarise our developmental work overt the last 15 years from studies in very simple organisms namely Danio Reiro (Zebrafish) and Drosophila Melanogaster (common fruit fly) to two well-described developmental rodent models, namely maternal immune activation and developmental vitamin D deficiency. The feature common to all experiments is the timing of exposure. In all organisms there appear to be critical early embryonic windows of exposure that produce persistent alterations in dopamine signaling in the resulting adult. Exposures outside of such windows produce no such effect.

In contrast to these developmental studies, relatively recent findings from Howes and colleagues have shown that dopamine systems in patients “at risk of developing psychosis” may also function abnormally in late adolescence or early adulthood prior to the onset of psychosis. This has stimulated us to consider if this so-called “prodromal” period also represents a particularly vulnerable time in a dopamine neuron’s journey towards psychosis. In the 2nd part of this talk I will summarise unpublished findings from our very latest model, “Enhanced Dopamine in Prodromal Schizophrenia” (EDiPs).

In summary we conclude that when considering the etiology of schizophrenia that rather than all roads leading to dopamine, perhaps, this may be where they start.

Directions to UQ

Google Map:
To St Lucia Campus, UQ Ipswich, and UQ Gatton.

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