Homeostatic plasticity is the response neurons undergo to regulate changes in excitability levels and bring the cells back to homeostasis. Research on homeostatic plasticity at the molecular level can lead to improved treatments for neurological diseases such as epilepsy, Alzheimer's, and schizophrenia. The research featured in this poster looks at the response of GIRK (G protein-gated inwardly rectifying potassium) channels and GABAb (gamma-amniobutyric acid) receptors to neurotoxins, tetrodotoxin (TTX) or bicuculline (BC).
Prolonged activity blockade of 48 hour TTX treatment significantly reduced GABABR1 and GIRK2 expression. This supports the idea that because these two proteins inhibit action potentials, there will be fewer of them found in the cell to offset the inhibition caused by TTX. However, there was no change in expression for GABABR2. In order to function, GABABR2 and GABABR1 rely on one another. Perhaps the decrease in GABABR1 expression is enough to offset the inhibition by TTX. Prolonged activity excitation of 48 hour BC treatment resulted in no significant change for GABABR1, GABABR2, and GIRK2 expressions. Although their expressions may not have changed, it is possible that their activity could still be increased.
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Hammer, Staci E.; Weiss, Amanda; and Chung, Hee Jung, "GIRK2 and GABABR1 Downregulate in Response to TTX as GIRK2, GABABR1, and GABABR2 Are Not Affected by BC Treatment" (2017). Phenotypic Plasticity Research Experience for Community College Students. 3.