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- mbing fiber depolarizes mbrane potential to en Ca2+ channels. tage-gated channel 2+ Ca²+ Release 2+ Ca²+ Endoplasmic reticulum removal of AMPA receptors from the postsynaptic membrane. insertion of AMPA receptors into the postsynaptic membrane O increase in intracellular Ca2+ via voltage-gated Ca2+ channels O DAG- and Ca2+-mediated activation of PKC increase in intracellular Ca2+ via endoplasmic reticulum IP3 receptorsThe membrane voltage in graded potentials can be produced by Oopen channels and ligand-gated chanels Ovoltage-gated channels Oligand-gated and mechanically gated channels Oligand-gated channels mechanically gated channelsAction potentials propagate in one direction because of: O K+ Voltage-gated Channels become inactive for a while O Nat Voltage-gated Channels become inactive for a while O K+ nongated Channels become inactive for a while O Nat nongated Channels become inactive for a while
- Which of the following statements best describes the features of voltage-gated K+ channels? They consist of 4 subunits, are activated at the same time as voltage-gated Na+ channels, but do not inactivate. They consist of 4 subunits, are activated by depolarisation and close slowly during the refractory period. They have 24 membrane spanning alpha helices, 4 of which have positively charged amino acids which promote a conformational change in the channel following depolarisation. They consist of 4 subunits and are open at rest which causes the resting membrane potential to be close to the K+ equilibrium potential.Both rhodopsin in vision and the muscarinic acetylcholine receptor in cardiac muscle are coupled to ion channels via G proteins. Describe the similarities and differences between these two systems.2) Describe the sequence of events that occur after a stimulus depolarizes the membrane from resting potential and exceeds threshold. Be sure to discuss the inactivation and activation of ion channels in relation to changes in membrane potential. 3) A key feature of voltage-gated ion channels is that they are regulated by two gates: activation gates and inactivation gates. Discuss how these gates regulate voltage-gated ion channel function.
- apucreceptors ava ble at the synapse are reflected in this number. Question 2: In this chapter, we discussed a GABA-gated ion channel that is permeable to Cl. GABA also activates a G-protein-coupled receptor called the GABA receptor, which causes potassium-selective B channels to open. What effect would GABAB receptor activation have on the membrane potential? GABAB receptor activation causes potassium-selective channels to open. As a result this bringhs theThree currents are produced by a 56 mV depolarization leading to an action potential in a squid axon membrane during a voltage clamp experiment as shown. What is the mechanism underlying the capacitive current? 56 mV Depolarization Capacitative current Late current Early current Time (ms) Opening of Na* channels Current due to the Na/K* pump O Neutralization of the charge on the membrane Opening of K channels Membrane Membeane current imA/cm potential (mV)Name and describe the roles of key molecules and membrane structures in maintaining axon membrane resting potential of-70 mV Name and describe the roles of key molecules and membrane structures in propagation of axon membrane action potentials during depolarization at +35 mV Explain why they myelin sheath of white matter neurons allows faster action potential transmission than that of neurons found in gray matter.
- Assume the membrane is only permeable to Na+ and K+, the electrical model of axon membrane is the following: Outside A INa gna ENa Ex D Inside The membrane potential at rest and at peak is -70mV and 45mV respectively; the potential of Sodium ion is 60mV and the potential of Potassium ion is -80mV. Find the ratio 9Na at rest and at peak. gKIPSP could result from :-a- opening of K + channelsb- opening of ligand-gated cation channelsc- closure of Cl- channelsd- closure of potential-gated Ca ++ channelsThe giant axon of the squid (Figure Q11–3) occu-pies a unique position in the history of our understandingof cell membrane potentials and nerve action. When anelectrode is stuck into an intact giant axon, the membranepotential registers –70 mV. When the axon, suspended in abath of seawater, is stimulated to conduct a nerve impulse,the membrane potential changes transiently from –70 mVto +40 mV.