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A somatic motor neuron forms a synapse with a skeletal muscle cell. You apply a voltage-gated calcium channel antagonist to the synapse, and it affects both cells in the synapse. This blocks the skeletal muscle cell from contracting. Explain why this occurs. Demonstrate your knowledge of both synaptic transmission and cell signaling within the skeletal muscle in your answer.

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4 Jun 2019
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Related questions

3. a) The neurotransmitter that is responsible for “communication” at the neuromuscular junction between motor nerve cells and skeletal muscle fibers is acetylcholine (ACh). The ACh receptor protein is a channel that opens when ACh binds. Upon the opening of this channel, the membrane at the motor end plate region of the muscle cell becomes depolarized, resulting in the generation of an action potential in the muscle fiber membrane. The ACh receptor channel is equally permeable to both Na+ and K+ ions. Explain how opening a channel that allows both potassium and sodium to cross the membrane results in membrane depolarization. (2 points)

b) In normal individuals, a single end-plate potential (EPP) is always sufficient to elicit an action potential (and hence contraction) in a skeletal-muscle fiber. This is not the case in individuals suffering from myasthenia gravis (MG). MG is an autoimmune disorder in which antibodies are produced that attack the AChRs at skeletal-muscle endplates reducing their number. Patients suffering from the disease present with significant muscle weakness. Explain why patients with MG would exhibit muscle weakness. (2 points)

c) Treatment strategies for myasthenia gravis include thymectomy (removing the source of the antibody producing cells) or immunosuppressant drug therapy (inhibiting the synthesis and release of the antibodies). In addition, the drug neostigmine administered at carefully monitored doses is highly effective in treating myasthenia gravis. Investigate the actions of neostigmine, and discuss in detail why it may be an effective treatment. (2 points)

The junction specialized for the transmission between a neuron and another cell is called a (1) _____ ______. Usually, the signal being sent to the receiving cell is carried by chemical messengers called (2) _____. (3) _____ is an example of this type of chemical messenger, which diffuses across the synaptic cleft, combines with protein receptor molecules on the muscle cell membrane, and soon thereafter is rapidly broken down by enzymes. At an (4) ____ synapse, the membrane potential is driven toward the threshold value and increases the likelihood that depolarization and an action potential will occur. At an (5) ____ synapse, the membrane potential is driven away form the threshold value, and the receiving neuron becomes hyperpolarized and is less likely to achieve an action potential. A specific transmitter substance can have either excitatory or inhibitory effects depending on which type of protein channel it opens up in the (6) ____ membrane. (7) ____ are neuromodulators that inhibit perceptions of pain and may have roles in memory and learning, emotional states, temperature regulation, and sexual behavior. (8) ____ ________ at the cellular level is the moment-by-moment tallying of all excitatory and inhibitory signals acting on a neuron. Incoming information is (9) ____ by the cell bodies, and the charge differences across the membranes are either enhanced or inhibited. Some narrow-diameter neurons are wrapped in lipid-rich (10) _______ produced by specialized neuroglial called Schwann cells; each of these is separated from the next by a(n) (11) ________ ________ - a small gap where the axon is exposed to extracellular fluid. A (12) ____ is an involuntary sequence of events elicited by a stimulus. During a (13) _______ ________, a muscle contracts involuntary whenever conditions cause a stretch in length; many of these help you maintain an upright posture despite small shifts in balance. Imbalances can occur at chemical synapses; a neurotoxin produced by Clostridium tetani blocks the release of GABA and glycine, thus freeing the motor neurons from (14) _____ control, which may cause tetanus – a prolonged, spastic paralysis that can lead to death. A. Excitatory H. Stretch reflex B. Inhibitory I. Summed C. Myelin J. Neurotransmitters D. Chemical synapse K. Postsynaptic E. Synaptic integration L. Endorphins F. Exposed node M. Acetylcholine (ACh)

A well-studied autoimmune and neuromuscular disease affects the neuromuscular junction of afflicted individuals. It turns out that antibodies attack the ligand receptor found on the skeletal muscle cells and reduces the number of these receptors, leading to weakness in eye muscles, facial muscles and in severe cases affects respiratory muscles.

In comparing the monosynaptic pathway for an individual without the disease and with the disease, if the sensory neuron in both individuals received the same stimulus (both in intensity and frequency), would the relative amount of neurotransmitter released at the neuromuscular junction differ? Why or why not (meaning explain using the physiology)? ( Would the end plate potential (EPP) differ in a person without the disease versus someone with this disease? How, explain

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