1. Ionotropic GABA receptors are ligand-gated Cl channels which open during GABA-ergicsignaling.a) Describe how under normal circumstances the opening of these channels leads to an IPSP.Do this in the context of Eci.b) Some cells in the body express a Na*/K+/2Cl cotransporter which pumps Cl- into the ICF.Where these pumps are present, the same GABA receptor is actually excitatory. Again, inthe context of Ea describe how the same receptor would be excitatory in cells which activelypump Cl- into the ICF. You do not need to repeat information you provided in part (a)

Introduction Neurons are specialized cells that are the basic building blocks of the nervous system.…

Answered: 1. Ionotropic GABA receptors are…

Human Physiology: From Cells to Systems (MindTap Course List)

9th Edition

ISBN:9781285866932

Author:Lauralee Sherwood

Publisher:Lauralee Sherwood

Chapter3: The Plasma Membrane And Membrane Potential

Section: Chapter Questions

Problem 7UC: Describe the contribution of each of the following to establishing and maintaining membrane...

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Clostridium tetani toxin blocks the exocytosis of GABA. A. What anatomical part of a pre-synaptic neuron would be affected by this? B. How would a post-synaptic neuron’s likelihood of experiencing an action potential be affected by this toxin? C. Explain, using at least TWO of the following terms: threshold, depolarization, repolarization, hyperpolarization, summation, IPSP, EPSP, exocytosis
Name a drug for treatment for overactive bladder syndrome which does not target the muscarinic M3 receptors directly, but rather targets one of the second messenger signalling molecules within the smooth muscle cells as a result of muscarinic M3 receptor activation. Which second messenger molecule would you choose to target? Justify your choice and explain how targeting this second messenger pathway would result in the reduction of bladder smooth muscle contraction.
explain in detail ephrin receptor EPHB2 receptor interaction with PDZ ligand. give full step by step explanantion.
The tight binding sites required for ion selectivity should slow the progress of ions through a channel, yet ion channels achieve rapid rates of ion transport. How is this paradox resolved?
Describe the contribution of each of the following to establishing and maintaining membrane potential: (a) the Na+K+ pump, (b) passive movement of K+ across the membrane, (c) passive movement of Na+ across the membrane, and (d) the large intracellular anions.
Design a novel drug for treatment for overactive bladder syndrome which does not target the muscarinic M3 receptors directly, but rather targets one of the second messenger signalling molecules within the smooth muscle cells as a result of muscarinic M3 receptor activation. Which second messenger molecule would you choose to target? Justify your choice and explain how targeting this second messenger pathway would result in the reduction of bladder smooth muscle contraction.
Describe the normal functioning of the Na-K pump, with special attention on how phosphorylation state affects ion binding affinity.
i. Write an equation balancing the electrical potential and chemical potential for 3 Na+ and 1 Ca2+. Note that NCX is an antiporter, whereas SGLT1 is a symporter, thus the maximal electrochemical gradient of Ca2+ will be opposite that of glucose. ii. Rearrange this equation in to give intra-cellular Ca2+ as a function of extra-cellular Ca2+, intra-cellular and extra-cellular Na+, resting membrane potential. You should note the equation and substitution below. iii. Use the values below for extra-cellular Ca2+, intra-cellular and extra-cellular Na+, resting membrane potential to calculate intra-cellular Ca2+. Extracellular Na+ concentration is 140mM, intracellular Na+ concentration is 12mM, extracellularCa2+ concentration 2.5mM, and the resting membrane potential is -65mV.
What molecule acts as a positive effector (activator) of ATCase? What molecule acts as an inhibitor?
Which patch clamp technique should be used if you want to investigate the effect a compound has presynaptically with varying concentration?
How does the activity of the sodium-potassium antiport pump contribute to an overall negative membrane potential of between -60 and -90 mV?
Interpret the effect of hyperkalemia with reference to Goldman’s equation. a) What happens to rate of K+ diffusion at the MRP equilibrium with elevated extracellular [K+] (and unchanged intracellular [K+])?b) Since this diffusion rate determines the “permeability” of the cell to that K+ ion, what happens to PK+ as a result of this elevated extracellular K+? (Hint- it HAS changed.)c) Since PK+ has changed, and PNa+ is unchanged, what happens to the MRP as a result of this change in PK+? Explain with specific reference to Goldman’s equation but there is no need to cite or calculate any specific numbers, just generalize the result.

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