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Tracking The Progression Of Defects At The Neuromuscular Junction In Huntington's Disease, Katherine A. Trittschuh
Tracking The Progression Of Defects At The Neuromuscular Junction In Huntington's Disease, Katherine A. Trittschuh
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Huntington’s disease (HD) is a genetic disorder associated with progressive cognitive and motor decline. Recent studies in HD models suggest primary peripheral pathologies arise independent of changes in the central nervous system. Our lab found defects in skeletal muscle occurring early in the progression of disease in transgenic R6/2 HD mice, resulting in membrane hyperexcitability. Additionally, there is evidence of decreased quantal content in late-stage R6/2 mice. Here, we investigate pre-synaptic and post-synaptic function at single neuromuscular junctions (NMJ) to make direct comparisons of disease progression in the muscle membrane and motor nerve terminal. We hypothesize that muscle membrane defects …
Osmotic Activation Of Sperm Motility Via Water Flow Through Aquaporins In The Freeze-Tolerant Cope's Gray Treefrog, Dryophytes Chrysoscelis, Deja Miller
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Gametes of gray treefrogs, Dryophytes chrysoscelis, are deposited into freshwater ponds. Sperm undergo spermatogenesis and maturation beginning in the seminiferous tubules and migrating to the lumen. In mammals and fishes, these cells are immotile within the isosmotic fluid of the testes and have motility activated by exposure to a hyper- or hypoosmotic medium. Water flows into or out of the sperm cell, altering intracellular ionic concentrations, and ultimately stimulates flagellar movement. We tested the hypothesis that exposure to a hypotonic environment activates motility of gray treefrog sperm. We also hypothesized that osmotic water uptake is facilitated by expression of water …
Fast Voltage-Gated Sodium Channel Currents And Action Potential Firing In R6/2 Skeletal Muscle, Eric Joshua Reed
Fast Voltage-Gated Sodium Channel Currents And Action Potential Firing In R6/2 Skeletal Muscle, Eric Joshua Reed
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Huntington’s disease (HD) is a degenerative disorder caused by expanded CAG repeats in the Huntingtin gene, which results in cognitive problems as well as muscle weakness, chorea, rigidity, and dystonia. Most research in HD has focused on neurodegeneration, but recent studies have found peripheral defects that may help explain the debilitating motor symptoms of HD. We have shown that skeletal muscle from the R6/2 transgenic mouse model of HD is hyperexcitable due to decreases in resting chloride and potassium currents. Other groups have speculated that the fast voltage-gated sodium channels may be affected in Huntington’s disease as well. To fully …