Table Q1(a) shows typical values for the intracellular and extracellular concentrations of the major ion species (in millimoles per litre) for frog skeletal muscle. Table Q1(a) Intracellular Permeability (cm/s) 2х 10% 2х 105 4 x 106 Ions Extracellular Na* 12 145 K* 155 4 4 120 By referring to Table Q1(a), compute the equilibrium resting potential for this membrane by assuming the room temperature is 20° C. Given the Boltzman's constant, k = 1.38 x 1023 J/K and an electronic charge, q = 1.602 x 10-19 C.
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- (a) Table Q1(a) shows typical values for the intracellular and extracellular concentrations of the major ion species (in millimoles per litre) for frog skeletal Q1 muscle. Table Q1(a) Permeability (cm/s) 2 x 10-8 2 x 106 4 x 10-6 Ions Intracellular Extracellular Na* 12 145 K* 155 4 4 120 By referring to Table Q1(a), compute the equilibrium resting potential for this membrane by assuming the room temperature is 20° C. Given the Boltzman's constant, k= 1.38 x 1023 J/K and an electronic charge, q = 1.602 x 1019 C.The ion flows across neuronal membranes at rest and duringan action potential do not significantly change bulk ionconcentrations, except for that of Ca2+ ions. Resting Ca2+ ionconcentrations in cells are usually about 10–7 M, and Ca2+ ionsexert physiological effects at concentrations of perhaps 10–5 M.Explain why relative changes of intracellular [Ca2+] are muchgreater than for, say, [Na+] (12–50 mM).Myasthenia gravis is a disease that leads to a marked decrease in the number of acetylcholine (Ach) receptors at the neuromuscular junction. As a result, suppose only about 200 (instead of 2000) Ach receptor-channels are opened by each quantum of Ach. The Ach-gated channels that survive operate normally and each cause a depolarization of about 0.25 x 10-3 mV when open. The function of the presynaptic terminal is normal and an action potential will cause the release of 100 quanta of neurotransmitter. Part a.) For a patient with myasthenia gravis, what would be the size (in mV) of a miniature excitatory post-synaptic potential (or that associated with one quantum of Ach)? a.) 0.05 mv b.) 0.25x10-4 mv c.) 0.25x10-3 mv d.) 0.5x10-3 mv e.) 0.5 mv Part b.) For a patient with myasthenia gravis, what would be the size (in mV) of the full excitatory post synaptic potential consequent to the entry of an action potential into the presynaptic terminal of the neuromuscular junction? a.) 70 mv…
- Myasthenia gravis is a disease that leads to a marked decrease in the number of acetylcholine (Ach) receptors at the neuromuscular junction. As a result, suppose only about 200 (instead of 2000) Ach receptor-channels are opened by each quantum of Ach. The Ach-gated channels that survive operate normally and each cause a depolarization of about 0.25 x 10-3 mV when open. The function of the presynaptic terminal is normal and an action potential will cause the release of 100 quanta of neurotransmitter. For a patient with myasthenia gravis, what would be the magnitude of the depolarization (in mV) associated with opening of one Ach-gated channel? a.) 0.25x10^-2 mv b.) 0.25x10^-3 mv c.) 0.25x10^-4 mv d.) 0.5x10^-1 mv e.) 0.5 mvNernst (equilibrium) Potential (mV) - 6.lol 0.07 0.125 D.094 lon Intracellular Extracellular Concentration (mM) Concentration (mM) K* 155 4 Nat 12 145 Ca** 104 1.5 4 120 D) If during the generation of an action potential in the skeletal muscle cell the membrane potential approaches +65 mV, membrane permeability for which ion likely plays a major role in membrane depolarization? Explain your choice.Calculate the equilibrium membrane potentials to be expected across a membrane at 37 ∘C, with a NaCl concentration of 0.50M on the "right side" and 0.08 M on the "left side", given the following conditions. In each case, state which side is (+) and which is (−). (a)Membrane permeable only to Na+.
- Intracellular potentials are on the order of -100mV, whereas extracellular potentials are OmV. Assuming these values, answer the following questions. (a) What is the electric potential energy of a chloride ion (CI-) inside a cell? (b) What about outside the cell? (c) What is the probability of finding a Cl- inside the cell relative to finding it outside the cell? Assume that T=310K. P(inside) P(outside) (d) If the concentration of Cl- outside the cell is 100mM, what is the expected concentration inside the cell?For a typical vertebrate cell with a membrane potential of −0.070 V (inside negative), what is the free-energy change for transporting 1 mol of Na+ from the cell into the blood at 37 °C? Assume the concentration of Na+ insidethe cell is 12 mM and in blood plasma it is 145 mM.Calculate the free energy of transport for the movement of potassium by the sodium/potassium pump under normal physiological conditions: 4 mM serum potassium, 135 mM intracellular potassium, 37.1 °C, and resting potential -82 mV. Express your answer in kJ/mol. Show all work. Calculate the free energy of transport for the movement of potassium by the sodium/potassium pump under disturbed conditions of 2 mM serum potassium. Assume all other parameters remain the same. Express your answer in kJ/mol. Show all work. What factors could limit the continued action of the sodium/potassium pump when only 2 mM potassium is present in the blood plasma? Note that under normal physiological conditions, the cell interior contains 11 mM sodium and the blood contains 140 mM sodium.
- Calculate the equilibrium membrane potentials to be expected across a membrane at 37 °C, with a NaCl concentration of 0.10 M on the “right side” and 0.01 M on the “left side”, given the following conditions. In each case, state which side is (+) and which is (-). (a) Membrane permeable only to Na+ (b) Membrane permeable only to Cl– (c) Membrane equally permeable to both ionsCompute the free energy change in Joules that occurs at 303 K as the cell is tranitions from resting state to the maximum depolarization potential. ● At resting state, the intracellular potassium and sodium concentrations are 140 mM and 10 mm, respectively. The extracellular sodium and potassium concentrations are 145 mM and 5 mM respectively.Below find the structures for ibogaine and cocaine. Ibogaine and cocaine inhibit the dopamine active transporter (DAT). This transporter is a secondary active transporter, and depends on the primary active transporter Na+/K+ ATPase. Ibogaine had a Kι = 2 μM, and cocaine a Kι = 0.64 μM respectively. (a) Define secondary active transport. (b) Is ibogaine an effective treatment for cocaine based on DAT binding?