Dr. McCluskey receives top honor for young taste researchers
Dr. McCluskey received the Ajinomoto Award for Young Investigators in Gustation during the 28th annual meeting of the Association for Chemoreception Sciences April 26-30 in Sarasota.
She was nominated by former mentor Dr. David Hill, neurobiologist at the University of Virginia in Charlottesville, who received the 1996 gustation award. Dr. McCluskey studied with Dr. Hill while earning her PH.D. in Virginia.
She got her first taste of gustation research in the late 1980s as an undergraduate at Florida State University. There another mentor, Dr. James C. Smith, a now-retired senior investigator, was the first to interest her in the complex system connecting thousands of taste buds on the tongue and palate with the brain.
"Receptor cells on your tongue are part epithelial cells: they turn over and they renew, and they are partly like neural cells, so they can fire action potentials and tell your brain about what is on your tongue," she says.
One of the most interesting – and fortunate – things about the system is that when communication with the brain is severed, nerves regenerate. "You can section a nerve and the taste buds go away but the whole thing regenerates and becomes functional again. I was really fascinated by the functional changes that you can see in this system even in an adult."
She hopes her studies of a system that successfully regenerates in the face of constant onslaught from the likes of food, teeth, bacteria and viruses will one day help nerves that are less successful at repair, such as those severed in a spinal cord injury.
"It's the flip side to the approach of looking at a spinal cord injury in an animal and seeing if you can reverse that. We chose to look at it a different way and say, 'Let's take a system that does regenerate pretty well and see what happens.'"
Her focus has become the role the immune system plays in recovery as she and others are learning more about how that system affects neurons and vice versa and how, as with any relationship, there are good and bad interactions.
Macrophages, one of the first immune cells to move in after an injury, seem to be a major player. The cells, known for their scavenging ability, also secrete nerve growth factors. "It turns out, if you don't have macrophages, you get deficiencies in neural function," says Dr. McCluskey, noting the finding is pretty amazing to many neuroscientists who have largely viewed the immune system as bad for neurons.
"We are trying to narrow down what molecules macrophages are secreting that are affecting taste receptors cells. Our goal is to show a definitive role for those cells and to also determine what other immune cells play a role," says Dr. McCluskey, who adds that for macrophages at least, that role may change over time following an injury.
She and her colleagues are starting with the adhesion molecules that summon macrophages circulating in the bloodstream to an injury site. "We are backtracking to the signals then that tell macrophages when to come into this area of injury and whether they just die, whether they exit, whether they proliferate, just what happens to these cells once they get the cue from dying cells."
Melissa Cavallin, an MCG graduate student Dr. McCluskey now mentors, recently received a National Institutes of Health predoctoral award to help elucidate these earliest interactions between injured taste buds and macrophages.
More recently, Dr. McCluskey's lab also began using the taste system as a model for poor nerve regeneration.
She has found that old healthy rats are not quite as good at functional taste bud regeneration as their younger counterparts.
Although most older people seem to have plenty of taste buds, they aren't quite so lucky with recovery from peripheral nerve injuries, such as a significant hand injury, which creates the opportunity for another model.
"It looks like in the older rats, the nerve cells don't functionally grow back," Dr. McCluskey says. She knows this is true out to 100 days, 60 days after a younger rat would have functional recovery. Apparently macrophage signaling is faulty or at least delayed in the older animals, a problem that may be replicated in the peripheral nervous system of older people. "If you sever a nerve in some place that should regenerate, it may be in aged people that it does not. So we want to set up a model where we can boost immune function, to see whether there are things we can do with growth factors to make these nerves regenerate in older rats as well. It looks promising," she says.
Dr. McCluskey's work is funded by the NIH's National Institute of Deafness and Other Communication Disorders.
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