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- Receptors, such as G-protein coupled receptors (GPCRs) are common drug targets.Ligands that target receptors are often characterised as being agonists orantagonists. Explain, with the aid of figures as appropriate, what these two termsmean.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).Which one of the cannot be considered a criterion when identifying a small neurotransmitter (NT)? T it must bind to postsynaptic receptor sites it can be isolated from the presynaptic cytoplasmic terminal O it is always released in a very predictable amount its biological activity can be terminated by enzymatic action
- Substrates for MAO (monoamine oxidase) include monoaminergio neurotransmitters cuch as catecholamines like dopamine (see image below): Н. NH2 HO Which do you think ls an Inhibitor for MAO? *NH2 Option 1 Option 2 don Option 3 Baced on the anower above, what type of Inhibitor le it? CompatitiveThe coincidence detector in presynaptic cells involved in classical conditioning and memory is. O adenylate cyclase O a calcium channel O a sodium channel O a potassium channelPart A Which of the following statements about pain-relief substances is correct? View Available Hint(s) O Endorphins are synthetic pain-killers. O Met-enkephalin has pain-killing ability because of its structural similarity to morphine. O Many natural pain-killing polypeptides are ideal for medical use. O Receptors of opium derivatives are found in all body cells. Submit
- 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.Excitatory neurotransmitters, example acetylcholine, effect firing of action potential. In contrast, inhibitory neurotransmitters, example, GABA suppresses firing of action potential. Based on your understanding of ion distribution across the membrane (more Na+ and Cl- outside; more K+ inside) and the mechanism of firing of an action potential, propose a molecular mechanism for the action of a tranquilizer drug -calming effect, example Valium. what is the most plausible mechanism for Valium and an alternative mechanism?Alcohol affects the central nervous system by enhancing the effect ofGABA at its receptor. GABA binds to GABA receptors and opensligand-gated Cl–channels. However, chronic consumption of alcoholmakes the GABA receptor less sensitive to both alcohol and GABA,which increases alcohol dependence as well as alcohol withdrawalsymptoms, such as anxiety, tremors, and insomnia. Benzodiazepinesenhance the binding of GABA molecules to their receptors and thus aresometimes used to treat people with alcohol withdrawal symptoms. Forsynapses involving GABA, predict the effect of alcohol on the postsynaptic membranes; compare the effect of chronic alcohol consumption onthe postsynaptic membranes in these synapses; and predict the effect ofbenzodiazepine treatment on the degree of polarization of postsynapticmembranes in people who are experiencing alcohol withdrawalsymptoms.
- 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+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 mvMyasthenia 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…