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The distribution of five Na,K-ATPase subunit isoforms (α1, α2, α3, β1 and β2) in rat cochlear and vestibular tissues was determined by immunocytochemical techniques using subunit isoform specific polyclonal antibodies. The expression of Na,K-ATPase α and β subunit isoforms varied among different cell regions of the inner ear. The α1 subunit isoform was more extensively distributed in all inner ear tissues than the α2 or α3 subunit isoforms. The β1 subunit isoform was distributed primarily in spiral ligament and inner hair cells of the cochlea, and in crista ampullaris and macula of the saccule. The β2, subunit isoform was most abundant in the stria vascularis, dark cells of the ampullae and utricle. The α1β1 subunit combination of Na,K-ATPase was most commonly found in the spiral ligament, while the α1β2 combination was most abundant in the stria vascularis. Similarly, α1β2 was confined more to the dark cells of the ampullae and utricle. The α3β1 suhunit combination of Na,K-ATPase was identified in the inner hair cells of the cochlea and the sensory regions of the vestibular end organs. These observations may reflect functional diversity of Na,K-ATPase in the individual inner ear regions and may provide insight into the differences between fluid and ion transport in the inner ear and that of other transporting tissues. Overall, the distribution pattern further indicates that the different isoform combinations have specific roles.

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by Wong Chi Shing Micky. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1996. / Includes bibliographical references (leaves 140-149). / Chapter Chapter 1. --- Introduction --- p.1 / Chapter 1.1 --- The Uterine Cervix --- p.1 / Chapter 1.2 --- Cervical Secretion and its Function --- p.3 / Chapter 1.3 --- Ion Transport System in Cell Volume Regulation --- p.6 / Chapter 1.3.1 --- "Regulatory Volume Decrease, RVD" --- p.8 / Chapter 1.3.2 --- "Regulatory Volume Increase, RVI" --- p.8 / Chapter 1.4 --- Signaling Pathways underlying RVD and RVI - The Role of Intracellular Free Calcium --- p.11 / Chapter 1.5 --- Swelling-induced Cl- Current --- p.12 / Chapter 1.6 --- Ca2+ activated K+ Channel --- p.14 / Chapter 1.7 --- Objectives of the Study --- p.15 / Chapter Chapter 2. --- Materials and Methods --- p.17 / Chapter 2.1 --- Materials --- p.17 / Chapter 2.1.1 --- Culture Media --- p.17 / Chapter 2.1.2 --- Chemicals --- p.17 / Chapter 2.2 --- Preparation of Solutions --- p.18 / Chapter 2.3 --- Cell Culture --- p.21 / Chapter 2.4 --- Patch-clamp Technique --- p.22 / Chapter 2.4.1 --- Preparation of Electrode --- p.27 / Chapter 2.4.1.1 --- Pulling and Polishing of Electrode --- p.27 / Chapter 2.4.1.2 --- Filling of the Electrode --- p.27 / Chapter 2.4.1.3 --- Coating of Electrode --- p.28 / Chapter 2.4.2 --- Patch-clamp Study --- p.29 / Chapter 2.4.2.1 --- Formation of Whole-cell Configuration --- p.29 / Chapter 2.4.2.2 --- Data Acquisition and Analysis --- p.31 / Chapter 2.5 --- Study of Cellular Volume Regulation by Confocal Laser Scanning Microscopy (CLSM) --- p.35 / Chapter 2.6 --- Determination of Intracellular Ca2+ by Confocal Laser Scanning Microscopy (CLSM) --- p.38 / Chapter Chapter 3. --- Results --- p.39 / Chapter 3.1 --- "Regulatory Volume Decrease, RVD" --- p.39 / Chapter 3.2 --- Responses of [Ca2+］i to swelling --- p.47 / Chapter 3.3 --- KC1 Efflux in RVD in HeLa Cells --- p.57 / Chapter 3.4 --- Swelling-induced Cl- Current --- p.67 / Chapter 3.4.1 --- Swelling-induced Anion and Cation Current --- p.67 / Chapter 3.4.2 --- Ca2+-independence of Swelling-induced Cl- Current --- p.71 / Chapter 3.4.3 --- Effect of Cl- Channel Blockers on Swelling-induced Cl- Current --- p.75 / Chapter 3.4.4 --- Anion Selectivity of Swelling-induced Cl- Current --- p.85 / Chapter 3.4.5 --- Cl- Dependence of Swelling-induced Cation Conductance --- p.85 / Chapter 3.4.6 --- K+ Independence of Swelling-induced Anion Conductance --- p.95 / Chapter 3.5 --- Ca2+ Activated K+ Current --- p.101 / Chapter 3.5.1 --- Ionomycin Induced Cell Shrinkage under Isotonic Condition --- p.101 / Chapter 3.5.2 --- Ionomycin Stimulated a Whole-cell K+ Conductance --- p.101 / Chapter 3.5.3 --- The Effect of Ionomycin on Intracellular Ca2+ Level --- p.111 / Chapter 3.5.4 --- Ca2+ Dependence of Ionomycin Stimulated K+ Current --- p.111 / Chapter Chapter 4. --- Discussion --- p.124 / Regulatory Volume Decrease in HeLa Cells --- p.124 / Role of Calcium in Regulatory Volume Decrease (RVD) --- p.126 / Swelling-induced Cation and Anion Conductance --- p.128 / Ca2+ Activated K+ Current in HeLa Cells --- p.134 / Chapter Chapter 5. --- Reference --- p.140

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Inanga (Galaxias maculatus) are a culturally and economically important fish species in New Zealand and abroad. However, very little is known about their ability to deal with trace element contamination. As a scaleless fish with the ability to survive in relatively extreme environments, they may not fit toxicity models (such as the biotic ligand model; BLM) based on other fish species. The aim of this study was to determine how this fish responds to elevated trace elements in both the laboratory and field in order to determine the applicability of these toxicity models. In order to determine the impacts of stress on ion transport and subsequent metal toxicity, inanga were exposed to handling stress and measures of ion uptake were collected. Handling stress was shown to result in increased ventilation rates, resulting in stimulated sodium (Na+) efflux. A compensatory increase in Na+ influx was also measured as a result of this stress. Inanga largely recovered from this ionoregulatory stress within 2 hours, with full recovery after 24 hours. This was indicative of a rapid homeostatic response for maintaining ion balance. Enhanced Na+ uptake in response to this stress resulted in increased copper (Cu) uptake in Cu-contaminated water, suggesting stressed fish will accumulate more Cu (and likely other Na+ mimics) than an unstressed fish. These results suggest a heightened vulnerability of inanga to this type of contaminant as a result of exercise stress during migrations. A combination of field and laboratory studies was used in order to measure trace element accumulation in inanga. In situ field studies showed changes to aluminum (Al) and iron (Fe) body burdens when inanga were placed in streams of varying trace element concentrations along the West Coast of the South Island. However, other trace elements measured did not alter over the period of exposure (9-10 days). Biochemical biomarker analysis showed no changes in the activity of Na+/K+-ATPase (NKA), but a marker of lipid peroxidation (thiobarbituric acid reactive substances; TBARS) was elevated in one stream. Analysis suggested that stream pH was the major driver of this effect, whether directly or via changes to metal bioavailability. Subsequent laboratory exposures (96 h) of inanga to 1.2, 2.7, 10.8, and 44 µg L-1 dissolved Fe and 5.6, 23.3, 60.7, and 128.7 µg L-1 dissolved zinc (Zn) showed no difference in whole body trace element accumulation, ammonia excretion, ion influx (Ca2+ and Na+), and TBARS. There were significant differences in oxygen consumption (MO2) after Fe exposures, with increases in the 2.7 and 44 µg L-1 dissolved Fe exposures. Laboratory exposure results suggest inanga are relatively insensitive to short-term Fe and Zn exposures. Both in vivo (whole body partitioning) and in vitro (Ussing chamber) techniques were used to determine the influence of cutaneous ion transport on preventing trace element accumulation. Results suggest inanga use their skin as an additional site of calcium (Ca2+) and Na+ uptake. This is the first study to confirm these ion transport capabilities in inanga, and revealed that up to 48% of Na+ uptake may occur across the skin. Pharmacological inhibition of Ca2+ uptake was achieved by known Ca2+ channel blockers (verapamil and lanthanum). Furthermore Fe and Zn impaired cutaneous Ca2+ transport, indicating that ion transport pathways in the skin modulate in response to these metals.