Aplysia is a popular organism being studied to demonstrate the roles of neurons and neural circuits in controlling human behaviors. For decades, Aplysia has been one of the most powerful structures for investigating cellular and molecular neurological mechanisms, especially neuroplasticity. Aplysia has been instrumental in analysis of molecular and cellular functions of numerous genes associated with human disease, making it more extensively researched than other organisms. Studies of the simple molluscan nervous system of Aplysia has led to improved approaches of many neurological disorders, including chronic pain, spinal cord injury, Alzheimer’s Disease and forms of dementia, Fragile X Syndrome, genetic learning disorders and more. Human society must acknowledge the impactful contributions of Aplysia to human society (2011, Aplysia).
There are many reasons Aplysia are an ideal subject for human neurological study. Aplysia‘s simple nervous system, contrasted with the complex neurological system of humans, as well as the ease with which Aplysia’s neuronal changes are observed to affect specific behavioral changes, have resulted in a rich succession of findings related to neuronal plasticity. Neuroplasticity is brain’s ability to repair or to re-wire itself (Martin, 2012). Neuroplasticity affects brain development from childhood through adulthood, as well as recovery from brain injury (Li et al., 2011). Aplysia are ideal for study because the simple nervous system, consisting of only nine ganglia with approximately 10,000 neurons. This means extremely large neurons can be accessed from the surface of the ganglion. Aplysia neurons have distinct colors and locations making them more identifiable, and analysis of short and long-term changes in structure and function of cells during specific behaviors has been beneficial in studying learning patterns. Aplysia possess non-associative and associative forms of long-term memory, and like humans they have simple learning patterns (habituation, sensitization, and conditioning). Aplysia remember a repeatedly trained gill-withdrawal response for up to three weeks, which is remarkable because the life span of Aplysia is only about one year, much shorter than the human lifespan, making it easier to study long term memory. Furthermore, mechanisms of long-term plasticity in Aplysia resemble that of humans, indicating a conservation of evolutionary events underlying learning and memory (2011, Aplysia).
The study of Aplysia has greatly contributed to advances in modern medicine. Here are some examples. In the 1960s, James Schwartz and Eric Kandel began establishing the biochemical and neuroanatomical learning and memory foundations, discovering that cyclic adenosine monophosphate (cAMP) is synthesized in Aplysia ganglia during short-term memory formation, and demonstrating that protein kinase effects on calcium channels are related to learned memory and behavior. In the 1980s, they discovered the necessity of protein synthesis for encoding long‐term memory (Robertson et al.,2010). Sensitization of Aplysia nociceptors displays similarities to changes in mammalian nociceptors associated with clinical chronic pain (Walters, 2009). Fragile X syndrome is a common form of mental retardation. Research confirms the Fragile X protein is essential for the brain’s ability to process sensory information, and children with Fragile X can be treated with behavioral therapy if started around 12 months old (Martin, 2012). We must acknowledge the importance of Aplysia to society and its benefits to neurobiological research.
References
(2011). Aplysia. Current Biology: CB, 21(2), R60-1.
Kandel, E. R. (2009). The Biology of Memory: A Forty-Year Perspective. The Journal of Neuroscience, 12748-12756. doi:10.1523/JNEUROSCI.3958-09.2009
Li, H. L., Miniaci, M. C., Kandel, E. R., & Choi, Y. B. (2011). A presynaptic role for FMRP during protein synthesis-dependent long-term plasticity in Aplysia. Learning & memory (Cold Spring Harbor, N.Y.), 18(1), 39-48. doi:10.1101/lm.1958811
Martin, B. S., & Huntsman, M. M. (2012). Pathological plasticity in fragile X syndrome. Neural plasticity, 2012, 275630.
Robertson, M., & Walter, G. (2010). Eric Kandel and Aplysia californica: Their role in the elucidation of mechanisms of memory and the study of psychotherapy. Acta Neuropsychiatrica, 22(4), 195-196. doi:10.1111/j.1601-5215.2010. 00476.x
Walters, E. T., & Moroz, L. L. (2009). Molluscan memory of injury: evolutionary insights into chronic pain and neurological disorders. Brain, behavior and evolution, 74(3), 206-18.
