Biomedical subjects

Gavin Dixon

Publications and source records attributed to Gavin Dixon.

4 recordsLinked to original sources

PubMed2006

No differences in calcium-binding protein immunoreactivity in the posterior cingulate and visual cortex: schizophrenia and controls.

UNLABELLED: Schizophrenia-specific alterations in the densities of interneurons immunoreactive (ir) to the calcium binding proteins are reported for several cortical regions. However, no reported studies have searched for such differences within the posterior cingulate cortex using antibodies to a specific calcium binding protein, calbindin (Cb). AIMS: Compare the (a) relative density of Cb-ir neurons (ratio of labeled neurons to total neurons), (b) relative width of cortical layers II/III and (c) somal areas of Cb-ir neurons in people with schizophrenia and non-psychiatric age-, gender- and postmortem index-matched controls (9 per group). METHOD: Tissue from Brodmann's area (BA) 30 and 23 and an internal control region, the visual cortex (BA 18) were labeled with polyclonal Cb antibodies then Nissl counter-stained. Cb-ir neurons as well as counter-stained neurons with clearly visible nucleoli were plotted and counted within their area 1 and laminar boundaries. RESULTS: No qualitative or statistical differences in the relative density of Cb-ir neurons were observed. A trend towards a significant effect was detected in BA 30, the relative density of Cb-ir neurons for controls was greater than for schizophrenics (P=0.0518). There were no significant differences in the relative cortical widths or somal areas. The data from this study suggest that the posterior cingulate cortex may not be involved in schizophrenia, at least not as far as Cb-ir neurons are concerned.

Adult↗

PubMed2004

No evidence for selective GABAergic interneuron deficits in the anterior thalamic complex of patients with schizophrenia.

Fewer neurons have been reported in the anterior thalamic complex (AT) of individuals diagnosed with schizophrenia in comparison to control tissue. In addition, the density of presumptive thalamo-cortical relay neurons of the AT is reported to be significantly decreased in schizophrenia compared with controls whilst total AT neuron density appears unchanged. We have investigated whether schizophrenia alters either the density of presumptive interneurons or the ratio between the two fundamental neuron types within the AT by immunohistochemically visualizing GABAergic neurons in post-mortem brain tissue from individuals with a diagnosis of schizophrenia pair-matched to tissue from normal individuals. Qualitative observations indicated no obvious differences between the two cohorts in the morphology of neurons exhibiting a GABAergic phenotype. A cell counting analysis of AT neurons revealed: (1) a non-significant 1% increase in density of GABAergic neurons in schizophrenia compared with controls and (2), a non-significant 6% increase in the percentage of neurons with a GABAergic phenotype in the schizophrenia group compared with controls. These findings suggest that a reduction of AT neuron number in schizophrenia does not alter either the morphology of neurons with a GABAergic phenotype or the ratio of neuronal phenotypes within AT.

Adult↗

PubMed2004

GABA transporters GAT-1 and GAT-3 in the human dorsolateral prefrontal cortex in schizophrenia.

This study aimed to investigate the binding affinity of [3H]GABA and [3H]beta-alanine to GABA transporters GAT-1 and GAT-3 in the human dorsolateral prefrontal cortex (Brodmanns' area 9) in schizophrenia. Using post mortem tissue from individuals diagnosed with schizophrenia (n=6) and control subjects (n=6), the density of GAT-1 was established by displacing [3H]GABA with muscimol, and for GAT-3 [3H]beta-alanine was used. Data analysis showed a significant decrease of GAT-1 levels (45%), and a significant increase of GAT-3 density (23%) within the dorsolateral prefrontal cortex of individuals diagnosed with schizophrenia when compared to age- and sex-matched controls. The observed decrease of GAT-1 could be explained as a consequence of the GABA hypo-function or the result of volumetric shrinkage of the cerebral cortex previously reported in this disease. The observed elevation of GAT-3 levels could be due to a compensatory effect for any functional loss of GABA re-uptake by the decreased GAT-1 levels.

Adult↗

PubMed2003

Neuropathological alterations in alcoholic brains. Studies arising from the New South Wales Tissue Resource Centre.

Alcohol dependence and abuse are among the most costly health problems in the world from both social and economic points of view. Patterns of drinking appear to be changing throughout the world with more women and young people drinking heavily. Excessive drinking can lead to impairment of cognitive function and structural brain changes--some permanent, some reversible. Patterns of damage appear to relate to lifetime alcohol consumption but, more importantly, to associated medical complications. The most significant of these is the alcohol-related vitamin deficient state, the Wernicke-Korsakoff syndrome (WKS), which is caused by thiamin deficiency but is seen most commonly in alcoholics. Careful selection and classification of alcoholic cases into those with and without these complications, together with detailed quantitative neuropathological analyses has provided data that gives clues to the most vulnerable regions and cells in the brain. Brain shrinkage is largely accounted for by loss of white matter. Some of this damage appears to be reversible. Alcohol-related neuronal loss has been documented in specific regions of the cerebral cortex (superior frontal association cortex), hypothalamus and cerebellum. No change is found in basal ganglia, nucleus basalis, or serotonergic raphe nuclei. Many of these regions which are normal in uncomplicated alcoholics are damaged in those with the WKS. Dendritic and synaptic changes have been documented in alcoholics and these, together with receptor and transmitter changes, may explain functional changes and cognitive deficits, which precede more severe structural neuronal changes. A resource to provide human brain tissues for these types of studies has been developed at the University of Sydney--the New South Wales Tissue Resource Centre. The aim of this facility is to provide research groups throughout the world with fresh and/or frozen tissues from well-characterized cases of alcohol-related brain damage and matched controls. The development of new technologies in pathology and molecular biology means that many more questions can be addressed using appropriately stored human brain tissues. Examples of the application of some of these techniques, involving neurochemical, neuropharmacological, neuroimaging and gene expression studies are included in this paper. Important public health outcomes have arisen from some of these studies including the enrichment of bread flour with thiamin for the whole of Australia. Researchers with an interest in alcohol studies can access tissues from this brain bank.

Alcoholism↗