Updated Post-Conference News: 2007 Nipissing University NRU Conference

Our lab is focused on the general problem of neural plasticity. We want to learn how the brain can express the malleability that is evident through exposure to various environments. In this search we have carried out numerous experiments and we have developed some notions on how environmentally mediated plasticity may be achieved in the brain. We also have a continuing interest in the toxic effects of neonatally administered compounds that may be especially toxic at early developmental stages. Most of our work in this area has focused on monosodium glutamate. We have shown, for example, that the behavioural deficits following early monosodium glutamate treatment can be ameliorated by "enriched" housing.
Lately, we have been investigating the role of brain structures in housing mediated neural plasticity. Using the oxidative metabolic enzyme cytochrome oxidase as a index of neural metabolism, we have found differential variations in metabolic capacity among brain structures as a response to enriched housing.
Recently, we have begun a series of lesion studies aimed at identifying brain structures most involved in attentional processes and thus in mediating housing related neural and behavioural plasticity. We began using ibotenic acid as the lesioning agent for the reticular thalamic nucleus. We then turned to 192-IgG saporin as a immunotoxic lesioning agent for central cholinergic systems, particularly the nucleus basalis. Our current research has been focused on somatostatin depletion in the brain. We have been given the chance to explore this area using somatostatin-saporin (courtesy of Dr. Douglas Lappi, Advanced Targeting Systems, California).

