The membrane potential in animal cells depends largely on resting K+ channels. How do these channels achieve selectivity for K+ versus Na+, which is actually smaller than K+?

What is the difference between a ligand-gated channel (like H1 or the AChR) and a voltage gated channel?

The membrane potential in animal cells, but not in plants, depends largely on resting K+ channels. How do these channels contribute to the resting membrane potential? Why are these channels considered to be nongated channels? How do these channels achieve selectivity for K+ versus Na+, which is smaller than K+?

Membrane potential in cells is constantly fluctuating. These fluctuations are called graded potentials and we will learn more about them in future lectures. Look at the fluctuating graded potential in the graph as an example. If Cl- generally has a relatively low membrane permeability, how would increasing Cl- permeability affect this graph?

Nernst (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.

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…

The top panel (a) of this figure shows the graded potential change (far right, upper, electrical trace) that results from ligand binding to the ligand gated Na+ channel. The bottom panel of this figure (b) shows a graded potential change (far right, lower, electrical trace) that results from ligand binding to a ligand gated Cl- channel. From this trace you know (Vm = -70 mV) 1. ECl- is -70 mV 2. ECl- is more negative than -70 mV (i.e., -80 mV) 3. ECl- is more positive than -70 mV (i.e., -60 mV)

For the ion concentrations in Table 12.1, calculate the equilibriumpotentials for each ion species in squid axons and in mammalianmuscle fibers.

Based on the same attached figure as in question 1 above (Figure 6.8A-B in your textbook) describing the NMDA receptor, a ligand-gated ion channel for glutamate, why does the current versus voltage response described by the red line go from near zero to a negative current at around -50 mV? (A) Channel pore Glutamate Mg2+ (B) EPSC (PA) 150 100 50 0 -50 -100 -150 Hyperpolarized, Mg2+ blocks ORA Glutamate + Mg2+ 0/ + Na Ca²+ Glutamate, no Mg2+ Depolarized, no Mg2+ block while K+ 100 Mg2+

The options for all 8 are either:  Depolarization, Na+ influx into cell Vm=-70mV inactivation of voltage-gated Na+ channels and opening of voltage-gated K+ channels Vm = -55mV, voltage Gated Na+ channels open graded potentials stimulating depolarization at the axon hillock hyperpolarization Repolarization, K+ efflux out of cell cells return to resting membrane potential