22 October 2019
Event date: 29 October
What: Associate Professor Kenneth Fish (University of Pittsburgh) on Region-, layer-, and cell type-specific GABAergic alterations in the cortical visuospatial working memory network in schizophrenia
When: Tuesday 29 October, 1-2pm
Where: Ian Potter Auditorium, Kenneth Myer Building, 30 Royal Parade Parkville
Host: Professor Anthony Hannan (firstname.lastname@example.org)
Details: For more information on this seminar or upcoming seminars in the series please contact email@example.com.
Web link: https://www.florey.edu.au/
Associate Professor Kenneth Fish Bio:
My research activities focus on the neuronal circuitry alterations that are associated with neurological and psychiatric disorders. The research strategies underlying these investigations incorporate, among other things, the macaque monkey, human post-mortem tissue, and advanced quantitative microscopy methodologies.
Specifically, macaque and human tissue is examined to establish the normal cellular components of the primate GABAergic and glutamatergic circuitry involved in behaviour (e.g., working memory). To extend findings generated under these studies, the developmental trajectories of these circuits are defined using a monkey developmental cohort.
Based on our findings, and those of others, hypotheses are generated regarding potentially dysfunctional circuit and cell type-specific alterations that are associated with a disorder (e.g., schizophrenia). To test these hypotheses, I’ve developed and/or refined over the past 20+ years multi-label immunohistochemical and multiplex fluorescence in situ hybridization assays and quantitative fluorescence microscopy techniques capable of extracting information on the GABAergic and glutamatergic synaptic architecture, mRNA expression, and relative protein levels in post-mortem tissue.
Tests of the cause-effect relationships among the neural circuit alterations associated with a given disorder, along with any potential influence medications might have on those circuits, are then performed in monkeys and rodents. The hope is that these studies will define pathogenic mechanisms that give rise to behavioural deficits of neurological and psychiatric disorders.