Researchers tackle disease that causes muscle spasms in animals
BY ALYSSA CALDER SPARK PROGRAM
A disorder that causes muscular spasms in many animal species is under the microscope of Guelph researchers who want to find the genes behind the disorder and methods to test for them. Knowing its causes, they believe, will help eliminate the disease through selective breeding.
Prof. Brad Hanna and graduate student Dan Finnigan of the Department of Biomedical Studies and Prof. Andrew Bendall, Molecular and Cellular Biology, are looking at domesticated animals such as cats, dogs, horses and Brazilian water buffalo (a food animal in its native country) to shed more light on myotonia congenita, a genetic muscle cell disorder that temporarily prevents muscles from relaxing after they contract. During these episodes, which usually last less than a minute, the animal shakes or shivers in place, unable to move.
Although the condition may be disturbing to a pet owner, it doesn't seem to do any damage to the muscle, says Hanna, so it often goes undiagnosed. But the problem is more serious in large animals. Prolonged muscular rigidity causes the animals to fall over as they try to move, which increases the risk of injury to both the animals and the people working around them. And it's undesirable in animal athletes such as race horses.
“Imagine a race horse that is unable to move out of the starting gate or cattle that stiffen and collapse when they're herded,” says Hanna.
He and Finnigan are focusing on how myotonia congenita works at the cellular level. In healthy animals, passageways in muscle cell membranes called chloride ion channels act as conduits for electrical nerve signals, which enter muscle cells and tell them to contract or relax. But animals afflicted with myotonia congenita have defective channels, causing muscles to contract but not relax right away.
That's where Hanna comes in. He's studying the ion channel function in animal patients suspected of having myotonia congenita. Currently, Finnigan and Bendall are using molecular biology techniques to look for mutations in the chloride ion channel genes. If a mutation is found, the genes responsible for the mutation are incorporated into cell cultures.
From there, Hanna can measure electrical currents in these cells to see whether the chloride ion channels are functioning properly. If they aren't, that means he and his colleagues may have found the mutation that causes myotonia congenita, which is the first step toward stopping the disease.
Hanna and Finnigan hope their research will lead to the development of blood tests for myotonia congenita, so breeders of cats, dogs, horses and livestock can eliminate the disease from their animals through selective breeding. As an added benefit, the researchers can also learn more about the relationship between structure and function of chloride ion channels in normal muscle, which could be of use to other muscle research in the future, Hanna says.
Also involved in this work are Profs. Joane Parent, Roberto Poma and Henry Staempfli and graduate student Ronaldo da Costa, Biomedical Sciences. This research is funded by the Morris Animal Foundation.
