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Explain the intracellular mechansim of smooth muscle relaxation of agaonist such as mepyrimine and atropine.
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- Explain the intracellular mechansim of smooth muscle relaxation of agaonist such as mepyrimine and atropine.Explain in detail Muscarinic receptors in regards to the hisamine agonist. How do they cause smooth muscle contraction. Provide mechanismDiscuss the similarities and differences by which Ca2+ activity is involved in initiating muscle contraction in skeletal versus smooth muscle fibers (hint: include Ca2+ sources, proteins it binds to, and signaling cascade it activates leading to contraction).
- Succinylcholine act as adepolarising agent that prevents repolarization of the somatic motor neuron. Thus, no further ACh is released until drug is cleared. Name another site within the MNJ we could target to prevent muscle contraction, and explain why this would work.Explain the structure of NMJ and name the steps of muscle stimulation in ordections in smooth muscle cells depend on which one of the following activation steps? Ca2+-activated phosphorylation of myosin-II Ca²+ binding to troponin GTP binding to myosin-II Actin polymerization (b) (c) (d) Explain:
- Describe in details the biochemical and mechanochemical series of events that enables motor neurons to trigger muscle contraction, using the biceps brachii as an example.Cardiac and skeletal muscle are both “striated” types of muscle and yet they have very distinct functional characteristics. a) Skeletal muscle functions as discrete motor units and the cardiac muscle works as a functional syncytium. Define the italicized terms in the previous sentence, explain their importance, and describe the cellular features that underlie these functional differences. b) Cardiac muscle exhibits automaticity, while excitation of skeletal muscle is neurogenic. Define the italicized terms and provide a brief explanation of mechanisms underlying each.In the rare neuromuscular disorder Myasthenia Gravis, autoantibodies are produced which inhibit acetylcholine receptor (nicotinic receptor) activity. Explain how inhibition of acetylcholine receptor activity at the neuromuscular junction will affect the sequence of events in muscular excitation and contraction in response to stimuli, and muscle function? (Mention the effects on all the significant events involved in excitation and contraction of muscles, and how it would affect muscle function).
- Why does muscle CAP Amp for both the normal Ringer's solution and Ringer's solution with Neostigmine increased as the stimulus amplitude increased, but a normal Ringer's solution would have a larger muscle CAP Amp value? Why is this the same case for a CAP Period as stimulus amplitude increases?. Why would Muscle CAP Period values for Ringer's with NEO then have larger values. Why does a normal Ringer's solution take longer to reach maximum action potential ?Discuss the formation of TMA in fish (explain further) How is TMA being regulated in the fish muscle? (explain further)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 mv