Abstract

It has been observed that the γ-amino butyric acid (GABA) receptor in possums reacts differently from that of placental mammals, in that GABA coupled with high salt intake leads to severe calcium imbalance and death. Thus, the potential of a marsupial-specific toxin (MST) was trialled on wild, captive possums. Seven groups of possums (n=13–15) were tested with mixtures containing 20% GABA and 2, 5 or 8% salt, with or without a chemical stressor, hydrocortisone, plus an untreated control group. Blood analyte data showed that plasma glucose concentration, measured by glucose oxidase method, increased in the control and hydrocortisone-treated possums. Ion homeostasis (potassium and sodium chloride, measured by ion-selective electrodes, and phosphate measured by phosphorus-colourimetric assay) was moderately affected in the MST-treated groups at higher salt concentrations. Calcium was affected in all but two of the treatment groups (2% and 8% plus hydrocortisone). Despite this disruption of ion homeostasis, there was no mortality due to the effect of the MST. This was possibly due to an aversion to the feed. Thus the development of an MST was unsuccessful.

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