Tenth Annual Grant Winners 2009-2010
Richard Dodge, Ph.D.
Richard E. Spieler, Ph.D.
Title: Evaluation of a New Animal Model for Gerontology Research
An aging population has provided an ever increasing interest in gerontology. Research in this field is undergoing explosive growth on both age-associated diseases and normal aging deficits. A major problem in gerontological research is finding appropriate vertebrate models for examining aging processes, both normal and disease states, as well as testing potential drugs and life-style changes that might beneficially alter these processes. Ideally there would be an animal model that had a similar aging process as humans allowing for rapid and inexpensive testing with large sample sizes. Recent literature indicates there may be such a model. There are some killifishes that only live one year or less (one species only 12-13 weeks). The animals undergo normal aging processes and senescence, including a host of physiological and cognative variables noted in mammals, during their short life-span. These small animals (<5 cm long) are easily bred and maintained in captivity. It is our intention to use the killifish as a model to pursue gerontological studies on learning and memory. Our studies will center on age-related changes in appetitive and aversive learning and memory processes in Nothobranchius furzeri using operant conditioned learning with a shuttle box. Both appetitive and aversive learning and memories show age-related changes. We will also correlate brain neurotransmitter levels with age and levels of learning and memory. It is noteworthy that the brains of bony fishes contain the basic blueprint, neuronal connections and same neurotransmitters, as mammals. Data resulting from the shuttle box and neurochemical testing will be subjected to relevant statistical analysis. This information will aid in judging the potential role of this animal model in gerontology research as well as provide important insight into age-dependent deficits in learning and memory and identify the neurotransmitters that are potentially involved in causing these deficits