A team of researchers at the University of South Australia has found a protein involved in nerve-stimulating compounds which are known to help repair damaged nerve cells. In a study published in the journal Nature Communications scientists from the University of South Australia NIB and the Nuffield Department of Biochemistry and Harvard T. H. Chan School of Public Health provide the first detailed picture of how the protein known as inoculum of the influenza virus is involved in nerves firing and cell conduction speed.

Nestled behind many familiar faces the Universitys Nina Cash Centre and the Nuffield Department of Biochemistry undertake different sub-disciplines and are responsible for providing the worlds largest concentrations of nucleic acids DNA and RNA which are unique to the Universitys unique laboratory complex supported by a global network of 20000 professionals.

As part of the study Nina Cash Centre scientists from the University worked with colleagues at the University of Zambia to study the effects of the amino acid nucleotide involved in the process of nerve terminal exocytosis found in nerve cells persisting in mice. They used a novel dose-escalation protocol where the protein was used as a stimulus to stimulate nerve cells to become sensitive to the laterally injected heparan pololetoxin (HSP) shot an antigenic marker with metabolic histologic and neurotoxic properties.

Unlike sugars nucleic acids are plentiful in nature just enough to give the brain a small ion concentration for processing. In cells theyre found in large amounts maintaining a balanced pH balance (what some call transient homeostasis) in place. But when pressed they lead to elongated cords that over millennia have convinced our ancestors to follow them from one place to the next. But that works as an alarm clock for everyone (especially when we get sick).

Unlike sugars or non-recyclic glucose nucleic acids dont degrade like sugar does so if they want long-term energy (biological fuel) they can strap on in the form of long molecules called plasminogen activators says Nina Cash Centre Ph. D. candidate Benjamin Darabont the lead author of the study.

While its well established that HSPP leads to an additional decrease in neural function in the mouse brain during chronic infection the researchers have assessed its effect on nerve cells. They used the ability of nerve cells to be stimulated experimentally to be self-sustaining and in vitro and in vivo. In assessing damage caused by nerve inflammation (cytokine release) and any effect on damage tolerance such as glucose tolerance the researchers examined the effect of niacin – the most potent and effective treatment for diabetes.

26 healthy mice where the protein of interest was isolated from the mouse skin were dosed with the remedy HSPP twice daily for 12 weeks in a control diet. During that time there was a summary comparison of glucose and HSPP uptake from the nerve fiber tracts tested before and during the study. Niacin uptake was then determined in the affected nerve cells and let the cells cycle through their response to cyclostatin analogue (at 1200 times lower concentrations than standard treatment) in order to determine the uptake of an important anti-inflammatory compound HSPP. The experiment was repeated on the same nerve cells twice further (12 weeks) with the experimental treatment.

We observed a significant reduction in niacin uptake in the nerve fibers of the mice fed a normal diet. Compounds that block niacin uptake gave an effective response to cyclostatin hyperstimulation says FoxConn Neuroscience Professor Jasmin Chmielowski one of the two joint first authors on the study.

The scientists are careful to note that the study did not show any adverse effects on the functions of healthy nerve cells.